In other studies, it was demonstrated that exposure of mouse podocytes to a combination of two circulating factors, i.e. suPAR and TNF, is sufficient to mimic some of the effects caused by exposure to serum or plasma from patients with REC of FSGS[14, 15], including an increased steady-state abundance of TRPC6 at the cell surface, the activation of alpha v beta 3 integrin signaling and decreased podocin expression. The gene discussed is NPHS2; the disease is focal segmental glomerulosclerosis.