Given that heterozygous COL4A3/COL4A4 mutations were observed in patients with familial FSGS 2, 4, and FSGS can be secondary to TBMN and AS 36, 37, 38, FSGS may be only a pathological lesion process in the related kidney diseases or secondary to the GBM pathology. This evidence concerns the gene COL4A3 and focal segmental glomerulosclerosis.