Reiser et al. [21] demonstrated a further five families with inherited FSGS who presented with heterozygous sequence changes in TRPC6. Overall 3 of the 6 described hereditary TRPC6 mutations caused increased Ca2+ influx when transfected into HEK293 cells [20,21], but importantly pathological effects were only observed in the kidneys despite widespread expression throughout the body. The gene discussed is TRPC6; the disease is focal segmental glomerulosclerosis.