In recent years, several studies on the pathogenesis of AD have found that the activation of T helper type 2 (Th2) inflammation-related pathways and its driving factors: interleukin (IL)-4, IL-13, and IL-31, as well as the sequential increase in the inflammatory dendritic epidermal cells, lead to altered cellular responses; thus, predisposing the patient to AD. This evidence concerns the gene IL31 and Alzheimer disease.