The “multi-hit hypothesis” is the current widely accepted framework for the pathogenesis of IgAN, in which a large amount of Gd-IgA1 characterized by the presence of galactose-deficient O-glycan in the hinge region is generated in the susceptible population after infection, and IgG autoantibodies targeting terminal N-acetylgalactosamine (GalNAc) residues following the deficiency of galactose in the hinge region on Gd-IgA1 are produced to form the IgG-Gd-IgA1 immune complex and deposit in glomeruli, mainly in the mesangium. The gene discussed is IGHA1; the disease is infection.