CD79A and glioblastoma: We hypothesize that the pathogenesis of patients with anti-GBM disease and IgA deposition in the mesangial region may be as follows: the patient begins with IgA deposition in the mesangial region, and the pathogenic circulating immune complex binds to type IV collagen in the mesangium of the glomeruli, changing the conformation of type IV collagen, exposing the α3 chain, and the patient produces anti-a3 (IV) antibodies, i.e., anti-GBM antibodies, which leads to the development of anti-GBM disease.