A number of gain‐of‐function mutations in TRPC6 result in autosomal dominant forms of focal segmental glomerulosclerosis (FSGS) (Heeringa et al., 2009; Reiser et al., 2005; Winn et al., 2005), and an increased abundance of glomerular TRPC6 proteins has been observed in patients with primary FSGS (Möller et al., 2009) and in animal models of glomerular disease (Kim et al., 2018; Staruschenko et al., 2023). This evidence concerns the gene TRPC6 and glomerular disorder.