Overproduction of inflammatory cytokines, such as interleukin-4 (IL-4), IL-13, and IL-31, particularly Th2 cells, is a characteristic of AD, and overproduction of cytokines is known to activate the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, which is the core of AD pathogenesis [5,6]. The gene discussed is IL31; the disease is Alzheimer disease.