IgAN is an autoimmune disease, and numerous studies have demonstrated that the pathogenesis of IgA involves the formation and deposition of immune complexes consisting of galactose-deficient IgA1 (Gd-IgA1) and autoantibodies against Gd-IgA1 (anti-Gd-IgA1 antibodies) in the glomeruli, along with activation of the complement system [5, 11–15]. The gene discussed is IGHA1; the disease is autoimmune disease.