A gain-of-function mutation in TRPC6 was identified as monogenic cause of FSGS, however, a small number of mutations with a loss-of-function TRPC6 phenotype have also been associated with FSGS (Riehle et al., 2016) and a novel heterozygous loss-of-function TRPC6 mutation was not associated with FSGS (Batool et al., 2023). Here, TRPC6 is linked to focal segmental glomerulosclerosis.