HEEs treated with IL-4, IL-13, and an alarmin, namely IL-25, recapitulated epidermal features of lesional AD such as a widening of the intercellular spaces (spongiosis) and dysregulated expression of AD biomarkers, including a decrease in FLG, LOR, and E-cadherin at the protein and/or mRNA levels, along with an increase in carbonic anhydrase 2, neural epidermal growth factor L-Like protein 2 and hyaluronic acid synthase 3 [105]. This evidence concerns the gene IL25 and Alzheimer disease.