Abstract
Mutations in the FLG gene, which encodes profilaggrin, are known to be a major risk factor for atopic dermatitis as well as other atopic diseases and systemic allergies. New research, however, shows that intragenic copy number variation within FLG also represents an independent risk factor for atopic dermatitis. The new findings indicate that upregulating FLG protein levels by 5-10% may have clinical utility in improving the management of many patients with dry skin and atopy.
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