AD pathogenesis involves multiple inflammatory cytokines, contributing to disease progression by promoting inflammation; these include interleukin 4 (IL-4), interleukin 13 (IL-13), interleukin 22 (IL-22), interleukin 31 (IL-31), thymic stromal lymphopoietin (TSLP), and interferon-gamma (IFN-γ) [8,9], which transduce signals through the Janus kinase–signal transducer and activator of transcription (JAK-STAT) signaling pathway, playing a critical function in regulating the immune response central to AD [10,11]. This evidence concerns the gene IL31 and Alzheimer disease.