Furthermore, they demonstrated that anti-PLA2R IgG4 autoantibodies could activate the MBL pathway in a glycosylation-dependent manner, leading to podocytes injury.[26] Li et al found that in the PLA2R-associated MN, the expression and intensity of glomerular MBL deposition was higher in the nephrotic syndrome group compared to the remission group, indicating that MBL deposition was correlated with non-remission.[27] While Zhang et al found that PMN patients with glomerular MBL activation can easily reach proteinuria incomplete remission (urinary protein 0.3–1.0 g/day). This evidence concerns the gene PLA2R1 and nephrotic syndrome.