The current body of evidence suggests that IgA nephropathy is an immune complex-mediated disease whose pathophysiology involves three immunological processes-excessive production of galactose deficient IgA1 by gut lymphocytes, followed by development of IgG autoantibodies against galactose-deficient IgA1, and mesangial deposition of immune complexes in the kidney superadded by the dysregulation of soluble CD89 (CD89 is an Fc receptor for IgA) and transglutaminase 2 [33,34]. The gene discussed is IGHA1; the disease is IgA glomerulonephritis.