FLG and inflammatory skin disease: Atopic dermatitis (AD) is a complex and heterogeneous inflammatory skin disease driven and modified by immunologic, environmental, and genetic factors.1,2 The identification of filaggrin (FLG) null alleles in up to 50% of patients with moderate-to-severe AD implicates a fundamental role for barrier homeostasis in this disease.3-6 Although the mechanisms leading to AD in FLG mutation carriers are unclear, the deficiency of FLG likely facilitates permeability of biologically active allergens and microbial colonization that subsequently trigger inflammatory cascades.7