In particular, mast cells play a key role in AD pathogenesis and are activated by cross-linking of the high affinity IgE receptor (FcεRI) and B cell-producing IgE, which results in the release of Th2 cytokines, IL-4, and IL-13, which induce phenotypic symptoms, such as the IgM to IgE switch, fibrosis, epithelial hyperplasia, and barrier dysfunction [2, 21]. This evidence concerns the gene IL4 and Alzheimer disease.