Loss-of-function mutations in the human filaggrin gene (FLG) have been identified as the major genetic predisposing factor for AD development,4, 5, 6 and in the context of the atopic march, patients with AD with FLG mutations are predisposed to the development of asthma.7, 8 We previously identified a mutation in the murine filaggrin gene (Flg) in the “flaky tail” double-mutant (Mattma/maFlgft/ft) mouse strain, resulting in a lack of filaggrin protein in the skin.9 The gene discussed is FLG; the disease is asthma.