Because of the links with Fyn, TGFβ and other TGFβ-related signaling molecules, such as Pcbp1[64], we speculate that Itch may function as a molecular rheostat, by regulating downstream TGFβ signaling (and FSGS pathophysiology) independent of ligand concentration. This evidence concerns the gene TGFB1 and focal segmental glomerulosclerosis.