With regard to the pathogenesis of IgA nephropathy, the 4-HIT hypothesis, including production of Gd IgA1 (Hit 1), IgG or IgA autoantibodies that recognize Gd-IgA1 (Hit 2), and their subsequent immune complexes formation (Hit 3) and glomerular deposition (Hit 4), has been widely supported by many studies [33]. The gene discussed is IGHA1; the disease is IgA glomerulonephritis.