Mutations in these genes (NPHS2, alpha-actinin 4 (ACTN4), Phospholipase C Epsilon (PLCE1), and Transient Receptor Potential Cation Channel Subfamily C Member 6 (TRPC6)) leads to the formation of FSGS, which is the most common form in SRNS patients [21-23]. The gene discussed is TRPC6; the disease is focal segmental glomerulosclerosis.