IgAN, a kind of primary glomerularnephritis that was first identified by Berger and Hinglais in 1968, represents the leading cause of kidney failure among East Asian populations.[15] Aberrant glycosylation of IgA1 elicits an autoimmune response, generating antiglycan antibodies.[16] Consequent immune complexes deposit in the glomerular mesangium, which activates the complement pathway, stimulates mesangial cells, and induces secretion of cytokines, finally resulting in inflammation and fibrosis. The gene discussed is IGHA1; the disease is kidney failure.