However, very recent data show that one defective TRPC6 gene copy is not sufficient to cause FSGS, which underscores the importance of increased rather than reduced calcium influx through TRPC6 for podocyte cell death.[32] In this context, pharmacological inhibition of TRPC6 channels (e.g., with SH045) may offer a promising therapeutic approach for chronic kidney disease, potentially mitigating maladaptive responses.[65]. Here, TRPC6 is linked to focal segmental glomerulosclerosis.