Only in recent years has the pathogenetic mechanism underlying IgA nephropathy been found, which can be divided into three essential steps: i) generation of abnormal IgA1 and formation of IgA1 complexes; ii) generation of mesangial injury mediated by interaction of IgA1 complexes with mesangial IgA receptors, and iii) progression of IgA-mediated mesangial injury towards renal failure [15], [16]. The gene discussed is IGHA1; the disease is IgA glomerulonephritis.