As a well-established Th2-dominant disease, AD pathogenesis involves hyperactivated JAK-STAT signaling (particularly JAK1-mediated pathways) in which IL-4 stimulation induces JAK1/JAK3 phosphorylation and subsequent STAT6 nuclear translocation, ultimately driving the expression of Th2-polarized genes in lymphocytes [15]. This evidence concerns the gene IL4 and Alzheimer disease.