Recent evidence has strongly suggested that IL-17-producing ILC3s drive colonic inflammation during Helicobacter hepaticus infection, and the number of NCR− ILC3s was significantly increased in the intestinal tract of colitis model mice, resulting in activation of mononuclear macrophages via secretion of IL-17 and other cytokines and then inducing a series of mucosal inflammatory responses [65, 66]. This evidence concerns the gene IL17A and colitis.