The pathogenesis of IgAN is characterized by the mesangial deposition of IgA1 immune complexes,[19] which is associated with a disordered mucosal-bone marrow immunity and initiates glomerular injury leading to glomerulosclerosis and tubulo-interstitial fibrosis.[2,20] Considering these pathologies, tonsillectomy might be useful for regulating the upstream of the disease via reducing aberrant IgA1, whereas corticosteroid therapy has the potential to ameliorate renal injury, the downstream of IgAN pathogenesis, by suppressing glomerular inflammation and fibrosis. Here, IGHA1 is linked to glomerulosclerosis.