NPHS2 and focal segmental glomerulosclerosis: In order to address the question whether TRPC6 dysregulation in podocytes is sufficient to drive development of FSGS, we have generated transgenic mice that overexpress the wild type protein or two mutated forms (P111Q and E896K, both previously described in FSGS patients) of Trpc6 channel under the regulation of the human podocin promoter (pNPHS2), which have been extensively used in other transgenic mice to direct expression exclusively to the podocytes [20]–[25].