Thus, environmental factors (e.g., climate, stress, antigens, microbiota, and pollution) or SNPs in non-immunological genes such as OVOL1 might alone or synergistically initiate a cascade of events leading to major lipid metabolism disturbances and epidermal barrier weakening, hence creating a favorable milieu for AD development in patients with susceptibility loci in immunogenic genes. Here, OVOL1 is linked to Alzheimer disease.