They further showed 23b−/− mice developed an IgA nephropathy-like phenotype of mesangial IgA and C3 deposition associated with the development of albuminuria, hypertension, and elevated serum creatinine, suggesting that loss of miR-23b is indispensably associated with IgA nephropathy [126] (Figure 2). This evidence concerns the gene CD79A and IgA glomerulonephritis.