Moreover, in the IgA nephropathy model induced by Sendai virus, mice deficient in C3aR and C5aR exhibited significant reductions in proteinuria, lower levels of renal IgA and C3 deposition, diminished histological damage, and decreased mesangial proliferation in comparison to wild-type mice (Zhang et al., 2017). This evidence concerns the gene C3AR1 and IgA glomerulonephritis.