Work undertaken in mice showed that filaggrin deficiency promotes AD-like symptoms in mice with a BALB/c background [183], in contrast to mice with a C57BL/6 background [186], showing that (1) filaggrin is a permissive but not an eliciting factor; and (2) other acquired factors, including immunological susceptibility, are important in AD pathogenesis. This evidence concerns the gene FLG and Alzheimer disease.