Dissecting the cause–effect relationships between the diseases and the genetic predisposition factors, including the loss of structural proteins (e.g., filaggrin (FLG)-deficiency (ichthyosis vulgaris—IV) in AD [27]) or unchecked TIR signaling cascades (e.g., hyperactivated caspase recruitment domain family member 14 (CARD14) in psoriasis [28]) may remind us of the premise that most ailments are products of gene–environment mismatches [29]. This evidence concerns the gene CARD14 and Alzheimer disease.