This suggests a potential association between PIG and the activation of a specific complement system on podocytes, possibly associated with podocyte injury disrupting matrix biosynthesis and degradation balance, and GBM thickening with increased permeability.[7,8] Feng et al[3] identified mutations in the INF2 gene, known for inherited focal segmental glomerulosclerosis (FSGS).[9–11] Additionally, a case report by Xiong et al[12] showed a novel SMARCAL1 mutation. This evidence concerns the gene INF2 and focal segmental glomerulosclerosis.