The finding that null alleles of the epidermis-expressed filaggrin (FLG) gene are a major risk factor for atopic dermatitis [52], and our observation that copy number variation of epidermis-expressed genes such as β-defensins and LCE3B/C predispose to psoriasis [51,55], indicate that epidermal biology and stratum corneum homeostasis play an important role in these common inflammatory diseases. Here, LCE3B is linked to atopic eczema.