Filaggrin Deficiency: The Core Protein Behind a Compromised Skin Barrier
Key Facts
- Roughly 10% of the general population, and 30-50% of individuals with atopic dermatitis, carry a heterozygous loss-of-function mutation in the FLG gene.
- Through hydrolysis, filaggrin releases amino acids and urocanic acid — the raw materials of natural moisturizing factor (NMF) — in the stratum corneum; these two products keep epidermal pH between 4.5 and 5.5.
- In individuals carrying an FLG mutation, transepidermal water loss (TEWL) values can run 2-3 times higher than healthy skin.
- Barrier repair formulations containing ceramides, cholesterol, and free fatty acids have been shown in clinical studies to significantly reduce TEWL linked to filaggrin deficiency.
- Filaggrin deficiency is recognized not just as a factor in atopic dermatitis, but as a systemic gateway in the "atopic march" that also raises the risk of allergic rhinitis, asthma, and food allergy.
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What Is Filaggrin, and What Does It Do in the Stratum Corneum?
To understand filaggrin, you have to look at the skin's outermost building block — the stratum corneum. This layer is made up of "corneocytes," the end product of keratinocytes' programmed death, and the lipid lamellae that fill the space between them. Filaggrin takes on two critical functions right at the center of this structure: it bundles keratin filaments together to provide mechanical rigidity, and then breaks itself down to form the source of natural moisturizing factors inside the corneocyte.Sandilands et al., 2009
Filaggrin's Chemical Conversion Chain
Profilaggrin → Filaggrin → Free Amino Acids + Urocanic Acid + Pyrrolidone Carboxylic Acid (PCA). When any link in this chain breaks, the NMF pool shrinks, corneocytes lose their water-binding capacity, and skin pH rises. That pH rise then over-activates serine proteases, accelerating desquamation and further disrupting barrier integrity.
The Bridge Between Filaggrin and the Skin Barrier
In the stratum corneum's "brick and mortar" model, corneocytes represent the bricks, while the lipid lamellae — the ceramide-cholesterol-fatty acid layers — represent the mortar. Filaggrin strengthens the model's "brick"; when it's deficient, the bricks loosen, the gaps between mortar layers widen, and a wide entry corridor opens up for allergens and irritants. Understanding the skin barrier's anatomy in depth also explains why filaggrin deficiency has such far-reaching consequences.
FLG Gene Mutations: The Genetic Basis and Prevalence
The most common cause of filaggrin deficiency is loss-of-function mutations in the FLG gene, located on chromosome region 1q21.3. These mutations were first identified by Palmer and colleagues in 2006, who established their strong link with atopic dermatitis.Palmer et al., 2006
The Most Common FLG Variants
| Mutation | Ethnic Distribution | Carrier Frequency (General Population) |
|---|---|---|
| R501X | European descent | 2-5% |
| 2282del4 | European descent | 2-4% |
| 3321delA | Japanese-Chinese descent | 1-3% |
| S3247X | East Asian | 1-2% |
| K4671X | South Asian | 0.5-1% |
The Difference Between Homozygous and Heterozygous Carriers
Homozygous carriers, who carry two mutant alleles, are predisposed to severe ichthyosis vulgaris, while heterozygous carriers, who carry a single allele, generally experience a milder but still chronic barrier fragility. Atopic dermatitis risk rises 3-5 times in heterozygotes; and because of the autosomal semidominant inheritance pattern from parent to child, family history is a strong risk indicator.
Non-Genetic Filaggrin Reduction
Even in individuals who don't carry an FLG mutation, filaggrin levels can drop due to various environmental factors: prolonged detergent exposure, excessive UV light, low ambient humidity, and Th2 cytokine dominance (IL-4, IL-13). IL-4 and IL-13 in particular directly suppress filaggrin gene expression; this mechanism explains the inflammation-barrier fragility vicious cycle seen in atopic dermatitis.Howell et al., 2007
The Link Between Filaggrin Deficiency and Atopic Dermatitis
Atopic dermatitis (eczema) is the inflammatory skin condition with the strongest genetic link to filaggrin deficiency established to date. That said, filaggrin deficiency isn't just a symptom of eczema — it's an independent risk factor associated with earlier-onset, more severe atopic dermatitis.Weidinger et al., 2007
The Atopic March Mechanism
Barrier dysfunction allows environmental allergens (dust mites, mold spores, food proteins) to reach epidermal Langerhans cells. This sensitization sets the stage for a strengthened systemic Th2 response through the bloodstream, elevated IgE, and the later development of allergic rhinitis and asthma. Early, effective intervention for filaggrin deficiency therefore has the potential to ease not just skin symptoms, but the long-term systemic atopic burden as well.
The Barrier-Inflammation Vicious Cycle
Filaggrin deficiency → rising TEWL → allergen penetration → Th2 inflammation → elevated IL-4/IL-13 → further suppression of FLG gene expression → the barrier worsens further. Breaking this vicious cycle requires targeting both inflammation and barrier repair at the same time. Our comprehensive guide on the relationship between eczema and the skin barrier details the practical management of this process.
Clinical Diagnostic Criteria and Barrier Measurement Methods
Immunohistochemical stratum corneum biopsy or genetic panel testing can be used to directly measure filaggrin deficiency. In everyday clinical practice, TEWL measurement (with a Tewameter) and corneometry (moisture content measurement) offer reliable functional indicators. Learning what TEWL means and how it should be interpreted is a critical starting point for making sense of filaggrin-linked barrier fragility.
The Concrete Effects of Filaggrin Deficiency on Skin
Beyond lab data, filaggrin deficiency profoundly affects skin's texture, appearance, and sensory responses. The table below summarizes the clinical reflections of these biochemical changes.
| Biochemical Change | Clinical Reflection | Affected Area |
|---|---|---|
| NMF reduction | Dryness, flaking | Face, palms, legs |
| Rising TEWL | Chronic dehydration sensation, tightness | Whole body, especially the antecubital fossae |
| pH rise | Excess serine protease activation, fine flaking | Face, neck |
| Lipid lamellae disruption | Redness, reactive sensitivity | Cheeks, forehead |
| Allergen penetration | Itching, eczema plaques | Inner arms, behind the knees |
| Microbiome imbalance | S. aureus colonization, infection risk | Flexural areas |
The Overlap Between Ichthyosis Vulgaris and Atopic Dermatitis
The large majority of individuals carrying a homozygous FLG mutation develop ichthyosis vulgaris (dry skin with a fish-scale appearance). In this presentation, the stratum corneum thickens while the normal desquamation chain becomes dysfunctional. Deepened palm creases (palmar hyperlinearity) and open, visible pores (keratosis pilaris) are also common accompanying findings of an FLG mutation.
Repairing the Skin Barrier: Science-Based Approaches
Since filaggrin deficiency has a genetic origin, changing the gene itself isn't currently possible; but functionally supporting barrier function is a scientifically proven, effective strategy. This support is essentially built on two axes: lipid replacement and humectants.Elias & Wakefield, 2019
Ceramide: The Core Building Block of the Lipid Lamellae
Making up roughly 50% of stratum corneum lipids, ceramide is one of the priority targets for barrier repair in filaggrin deficiency. When the physiological ceramide:cholesterol:free-fatty-acid ratio (around 1:1:1) is maintained, the lipid lamellae regain a tight structure. Detailed information on ceramide's place in skin chemistry offers a decisive guide for choosing the right product.
The Often-Overlooked Role of Cholesterol Support
When cholesterol isn't added to ceramide-centered formulations, barrier repair can slow down. Cholesterol regulates phase fluidity in the lipid lamellae, helping ceramides and fatty acids settle into the correct crystalline order. Learning more about cholesterol's role in skin barrier chemistry will make formulation choices more informed.
Humectants and NMF Support
Glycerin, hyaluronic acid, and urea (at low concentrations, 5-10%) supplement the NMF pool from outside, raising the stratum corneum's moisture content. Urea also has a keratolytic property that reduces buildup-related flaking and eases the ichthyotic appearance linked to filaggrin deficiency.
The CIRÈLL Biomimetic TriBarrier System and Filaggrin Deficiency
The Biomimetic TriBarrier System developed by CIRÈLL addresses barrier repair in filaggrin deficiency across three simultaneous layers: (1) Lipid Layer — a combination of physiological ceramides, cholesterol, and free fatty acids at ratios close to the stratum corneum's original stoichiometry; (2) Moisture Retention Layer — multi-layer humectants that mimic NMF; (3) Anti-Inflammatory Layer — plant-based and synthetic actives that calm Th2-driven inflammatory signals. This three-part approach offers an integrated solution to barrier fragility in filaggrin deficiency that goes beyond simple moisturizing.
A Care Routine for Filaggrin Deficiency: A Practical Guide
Managing barrier fragility linked to filaggrin deficiency requires not just the right active choices, but the right application order and habits too. The step-by-step protocol below is built on clinical dermatology and dermocosmetic research.
Cleansers containing sodium lauryl sulfate (SLS) suppress both filaggrin expression and ceramide synthesis. Sulfate-free gel or lotion formulas kept at pH 4.5-5.5 should be preferred. Water temperature shouldn't exceed 37°C, and the face shouldn't be in contact with water for more than 30 seconds.
A light toner containing glycerin (5-10%), panthenol, or beta-glucan is the precursor to the moisturizing layer. Alcohol-based toners should be avoided entirely; ethanol directly suppresses filaggrin expression. You can learn more about panthenol's mechanism for supporting the skin barrier.
At this stage, concentrated formulations of barrier-supporting actives like niacinamide (4-5%), madecassoside, or ectoin can be applied. Niacinamide stimulates ceramide synthesis and reduces TEWL; madecassoside supports type I collagen production while calming inflammation. Strong acid-based (low pH) serums should be used carefully in this skin type, or postponed.
An emollient moisturizer containing ceramides, cholesterol, and free fatty acids is applied at this stage. Applying to damp skin (3-5 minutes after cleansing) allows the lipid lamellae to organize more effectively while in a water-containing state. You can refer to our comprehensive guide for all the details of a barrier repair routine.
UV radiation suppresses filaggrin expression and directly weakens barrier function. SPF 30-50+ with UVA protection (PA+++ or higher), whether physical or hybrid-filter sunscreens, is mandatory for individuals with filaggrin deficiency. Mineral filters (zinc oxide, titanium dioxide) are better tolerated by sensitive skin.
The skin enters a repair cycle during sleep; TEWL runs roughly 25% higher overnight compared to daytime. This is why a night moisturizer can be more occlusive and nourishing than a daytime product. Biocompatible oils like squalane are excellent complementary occlusives for the night routine.
Practices to Avoid
- Hot showers and baths (shouldn't exceed 10 minutes, below 40°C)
- Irritating ingredients: SLS, fragrance, MI/MCI preservatives
- Over-exfoliation: AHA/BHA shouldn't be used more than 1-2 times a week
- Low-humidity environments: room humidity should be kept in the 40-60% range
- Soap bases (high pH) hiding in expensive "natural" cleansers
Environmental Factors and Seasonal Management
Individuals with filaggrin deficiency show unusual sensitivity to environmental changes. Even though the genetic basis stays fixed, environmental triggers can noticeably increase barrier fragility.Cork et al., 2009
Winter: The Most Critical Period
Cold air lowers humidity content; indoor heating systems can pull ambient humidity below 20%. Under these conditions, the TEWL spike runs more severe in individuals with filaggrin deficiency. Moisturizing frequency and occlusiveness should be increased in winter; using a humidifier in heated rooms can also be considered.
Summer: Sweating and pH Balance
Heavy sweating temporarily raises stratum corneum pH and can trigger excess serine protease activation. Excessive sun exposure, meanwhile, accelerates barrier loss through UV's filaggrin-suppressing effect. Light, non-comedogenic emollients and high SPF should be prioritized during this period.
Pollution and Urban Exposure
Particulate matter (PM2.5) and ozone suppress filaggrin and ceramide synthesis through oxidative stress. Polycyclic aromatic hydrocarbons (PAHs) also downregulate FLG gene expression via the aryl hydrocarbon receptor (AhR). Antioxidant-containing formulations (niacinamide, vitamin E, vitamin C) can partially offset this effect.
What Do These Skin Signals Mean?
Barrier fragility linked to filaggrin deficiency reveals itself through a number of distinct signs; recognizing these signs is the first step in determining the right intervention strategy.
The shrinking NMF pool in filaggrin deficiency pulls stratum corneum moisture content far below normal levels (20-35%). This shows up as an all-day dryness and restrictive tightness that doesn't clear even with moisturizer.
When the barrier is disrupted, irritants (fragrance, acid, cold air) easily reach nerve endings. This neurogenic-inflammation-triggered redness and burning sensation is among the most common functional complaints of filaggrin deficiency.
Serine proteases (KLK5, KLK7), made hyperactive by rising pH, break down corneodesmosomes prematurely, causing abnormal, visible desquamation. This flaking becomes especially noticeable around the sides of the nose, the eyebrows, and the cheekbones.
In filaggrin deficiency, production of antimicrobial peptides like defensin and cathelicidin also drops. When barrier gaps combine with reduced antimicrobial defense, Staphylococcus aureus colonization becomes easier; this worsens atopic dermatitis and sustains the itch-scratch cycle.
Conclusion
Filaggrin deficiency is a barrier fragility condition with a strong clinical and genetic basis that can't simply be dismissed as "dry skin." FLG mutations drain the epidermis's NMF pool, dramatically raise TEWL, and leave skin defenseless against allergens and irritants. Because all of these processes feed into each other in a vicious cycle, intervention must target both lipid replacement and inflammatory control mechanisms at the same time.
CIRÈLL's Biomimetic TriBarrier System aims to close this gap by rebuilding the physiological balance of ceramides, cholesterol, and free fatty acids; to raise stratum corneum moisture content by supplementing NMF from outside with humectants; and to ease Th2-driven barrier suppression with anti-inflammatory actives. Our comprehensive guide to managing atopic skin walks through how to put this strategy into practice step by step. You may not be able to change your genetic basis, but with the right knowledge and product choices, you can substantially improve barrier function.
Frequently Asked Questions
What is filaggrin deficiency — can you explain it simply?
Filaggrin deficiency is a condition in which filaggrin — a "filament aggregating protein" found in the skin's outermost layer (the stratum corneum) — is either insufficiently produced or loses its function. This protein normally holds keratin fibers together to provide mechanical integrity and, through hydrolysis, releases the raw materials of natural moisturizing factors (NMF). In filaggrin deficiency, both functions break down at once: the skin can neither retain moisture nor defend itself against external allergens and irritants. The result is chronic dryness, itching, and recurring periods of inflammation.
Is filaggrin deficiency hereditary? How does it develop?
The most common cause of filaggrin deficiency is loss-of-function mutations in the FLG gene, located on chromosome region 1q21.3. These mutations follow an autosomal semidominant inheritance pattern — meaning even inheriting a mutant allele from just one parent can cause barrier fragility. But even in individuals who don't carry a genetic mutation, an increase in Th2 cytokines like IL-4 and IL-13, UV exposure, SLS-containing cleansers, and low ambient humidity can suppress filaggrin expression and cause a functional deficiency. So filaggrin deficiency can have both a genetic and an environmental origin.
What's the relationship between filaggrin deficiency and atopic dermatitis?
FLG gene mutations are the strongest genetic risk factor identified to date for atopic dermatitis (eczema). While 30-50% of individuals with atopic dermatitis carry an FLG mutation, that rate sits around 10% in the general population. The mechanism works like this: filaggrin deficiency → barrier gap → allergen penetration → Th2 immune response → increased IL-4/IL-13 → further suppression of FLG expression. This vicious cycle is the core reason atopic dermatitis becomes chronic. FLG mutations are also recognized as an independent risk factor for allergic rhinitis and asthma.
How much do TEWL values rise in filaggrin deficiency?
Transepidermal water loss (TEWL) is one of the most reliable functional indicators of filaggrin deficiency. While TEWL runs 5-10 g/m²/hour on healthy skin, it can rise 2-3 times to 15-30 g/m²/hour in individuals carrying an FLG mutation with barrier dysfunction. During active atopic dermatitis flares, it can rise above 30 g/m²/hour. TEWL measurement is performed at a dermatology clinic with a Tewameter or similar device, and is also used to track the effectiveness of barrier repair treatment.
Which moisturizing ingredients should be used for filaggrin deficiency?
Moisturizer choice for filaggrin deficiency should be built on three main categories: (1) Emollients — physiological lipids like ceramides (particularly Ceramide NP, AP, EOP), cholesterol, and linoleic acid rebuild the lipid lamellae; (2) Humectants — glycerin (5-10%), hyaluronic acid, panthenol, and urea (5-10%) supplement the NMF pool from outside; (3) Occlusives — petrolatum, squalane, or beeswax form a protective film over the barrier, slowing moisture evaporation. Clinical studies support that formulations with a ceramide:cholesterol:free-fatty-acid ratio close to 1:1:1 deliver the most effective results in barrier repair.
Which skin types does filaggrin deficiency occur in more often?
While filaggrin deficiency can occur in any skin type, the clinically most pronounced presentation shows up in dry and atopic skin types. Genetic FLG mutation carriers exist in every ethnic group, but carrier frequency is higher in individuals of Northern European and East Asian descent. Even in normal skin, environmental triggers (SLS-containing products, low humidity, UV) can temporarily lower filaggrin levels. Functional filaggrin deficiency is less common in oily and combination skin types, but localized barrier fragility outside the T-zone is still possible in these skin types too.
When and how does filaggrin deficiency show up in children?
Barrier fragility linked to an FLG mutation usually shows itself from the first months of life. Dry, scaly, red skin patches appearing on the cheeks, forehead, and the extensor surfaces of the arms and legs are an early sign of infant eczema. During breastfeeding, the mother's diet and the ingredients in products applied to the baby's skin can shape this picture. Some clinical studies have shown that early, regular emollient use delays or eases the development of atopic dermatitis in babies carrying an FLG mutation. Infant atopic dermatitis is a process that also requires monitoring for later development of allergic rhinitis and asthma.
Does filaggrin deficiency progress differently in older adults?
Filaggrin and profilaggrin expression naturally decline with aging, which is why individuals over 60 can experience age-related barrier fragility even without carrying an FLG mutation. Post-menopausal estrogen decline is another factor that negatively affects filaggrin synthesis. In this age group, dryness, fine lines, and sensitivity are seen together. Urea-containing moisturizing creams (10-20%) are especially effective at supporting barrier function by correcting age-related hyperkeratosis. Very strong retinoid use should be approached carefully, since it can lower filaggrin and ceramide levels.
Why does filaggrin deficiency get worse in winter?
Cold, low-humidity air quickly lowers the stratum corneum's water content. When indoor heating systems pull ambient humidity below 20%, the rise in TEWL accelerates. Because this natural moisturizing mechanism is already impaired in individuals with filaggrin deficiency, barrier fragility noticeably deepens during winter. Additionally, friction under thick clothing and air-conditioning exposure while traveling also add to barrier stress. Increasing daily moisturizer frequency, switching to an occlusive at night, and using an ambient humidifier are the most practical precautions during this period.
Do ceramide-containing products really work for filaggrin deficiency?
Yes, strong clinical evidence shows that ceramide-based formulations meaningfully reduce TEWL linked to filaggrin deficiency and improve symptoms like itching and dryness. Ceramide makes up roughly 50% of stratum corneum lipids; to offset the ceramide loss that accompanies filaggrin deficiency, products formulated at physiological ratios (ceramide:cholesterol:free-fatty-acid around 1:1:1) should be preferred. Among ceramide types, NP (non-hydroxysphingosine) and EOP (eicosasphing-4-eninphosphoethanolamine) are among those that most closely mimic human skin lipids. But ceramide alone may not be enough; without support from cholesterol and fatty acids, barrier repair can remain incomplete.
Can AHA/BHA acids be used with filaggrin deficiency?
Acid exfoliation requires a high level of caution in individuals with filaggrin deficiency. Low-concentration AHA (5% or under glycolic or lactic acid) can improve barrier function in some individuals by clearing abnormal flaking caused by dead cell buildup. But high concentration or frequent use (more than twice a week) thins the stratum corneum, raises TEWL, and can suppress filaggrin and ceramide synthesis. BHA (salicylic acid) is better tolerated in oily areas but carries an irritation risk in dry and sensitive areas. Avoiding acid-containing products is recommended during periods of active inflammation (atopic dermatitis flare-ups).
Which ingredients cause side effects in filaggrin deficiency?
Ingredients individuals with filaggrin deficiency should pay particular attention to include: (1) SLS (sodium lauryl sulfate) — suppresses ceramide and filaggrin synthesis; (2) Synthetic fragrance and perfuming agents — can easily create systemic sensitization through a barrier with increased allergen-penetration capacity; (3) Alcohol denat/ethanol — directly suppresses filaggrin expression; (4) MI/MCI (methylisothiazolinone) — has a high rate of allergic contact dermatitis in dry and atopic skin; (5) Strong AHA-based chemical peels — over-thin the stratum corneum; (6) High-concentration retinol — can increase barrier stress during the initial period.
When should I see a dermatologist for filaggrin deficiency?
Seeing a dermatologist is recommended in the following situations: chronic, widespread eczema plaques that don't improve within 2-4 weeks of emollient use; signs of infection on the skin like yellow crusting, weeping, or cracking; itching severe enough to disrupt sleep quality; a rash around the eyes, eyelids, or behind the ears; a flare-up coinciding with a child's growth development; suspected sensitivity to multiple food or environmental allergens; regular steroid cream use lasting longer than 2 weeks. Some of these situations need to be managed with specialist-directed systemic or local pharmacological treatment.
In what order should cosmetic products that support filaggrin deficiency be applied?
The right application order is a critical factor in determining effectiveness. The recommended order is: (1) Wash the face with a sulfate-free, pH-balancing cleanser; (2) A light humectant toner or essence (glycerin- or panthenol-based) — onto damp skin; (3) An active serum (containing niacinamide, madecassoside, or ectoin) — still onto damp skin; (4) An emollient moisturizer containing ceramides, cholesterol, and fatty acids — 3-5 minutes after cleansing; (5) During the day: SPF 30-50+ sunscreen; at night: a squalane or occlusive beeswax layer. This order is also known as the "wet-on-wet" method, and it allows the lipid lamellae to organize more effectively while in their water phase.
How effective are cosmetics in managing filaggrin deficiency and eczema — is medication needed?
For mild-to-moderate barrier fragility linked to filaggrin deficiency, well-chosen cosmetic and dermocosmetic products are a primary treatment option; clinical studies show that regular emollient use significantly reduces the frequency and severity of atopic dermatitis flares. In severe atopic dermatitis, secondary infection, or accompanying systemic atopy (asthma, allergic rhinitis), topical corticosteroids, topical calcineurin inhibitors, or biologic treatments (like dupilumab) may be needed. CIRÈLL's barrier repair formulations can also be used effectively as adjuvant care alongside these pharmacological treatments; but a dermatologist should always be consulted during periods of active inflammation.
How does the skin microbiome get affected by filaggrin deficiency?
Filaggrin deficiency negatively affects the skin microbiome through several mechanisms. First, rising stratum corneum pH creates an optimal growth environment for Staphylococcus aureus while suppressing protective commensals like Staphylococcus epidermidis and Cutibacterium acnes. Second, reduced defensin and cathelicidin levels weaken antimicrobial defense. Third, the barrier gap acts as a direct entry point for outside pathogens. S. aureus colonization contributes both to worsening atopic dermatitis and to progressive sensitization; this is why probiotic-containing topical products that support the microbiome can also be considered as part of managing filaggrin deficiency.
Mine Ekber
CIRÈLL Formulation & Content Team
A content editor who works with the CIRÈLL R&D team on skin barrier physiology. The scientific claims on this page are based on peer-reviewed sources verified through PubMed/NCBI; the source list is below.
Scientific Sources
- Sandilands A, Sutherland C, Irvine AD, McLean WH. Filaggrin in the frontline: role in skin barrier function and disease. J Cell Sci, 2009.
- Palmer CN, Irvine AD, et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet, 2006.
- Howell MD, Kim BE, Gao P, et al. Cytokine modulation of atopic dermatitis filaggrin skin expression. J Allergy Clin Immunol, 2007.
- Weidinger S, Rodríguez E, Stahl C, et al. Filaggrin mutations strongly predispose to early-onset and extrinsic atopic dermatitis. J Invest Dermatol, 2007.
- Elias PM, Wakefield JS, Man MQ. Moisturizers versus Current and Next-Generation Barrier Repair Therapy for the Management of Atopic Dermatitis. Skin Pharmacol Physiol, 2019.
- Cork MJ, Danby SG, Vasilopoulos Y, et al. Epidermal barrier dysfunction in atopic dermatitis. J Invest Dermatol, 2009.
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