Blocking TRPC6 calcium channels appears to preserve podocyte function and prevent glomerular scarring in focal segmental glomerulosclerosis, a progressive kidney condition affecting the organ's filtering units. The mechanism involves preventing excessive calcium influx that triggers podocyte injury and subsequent nephron loss. This targeted approach represents a significant departure from current FSGS management, which relies primarily on immunosuppressive drugs that carry substantial side effects and often fail to halt disease progression. TRPC6 inhibition could address the root cause of podocytopathy rather than merely suppressing inflammatory responses. The therapeutic potential extends beyond FSGS to other proteinuric kidney diseases where podocyte dysfunction drives pathology. However, translating this mechanistic insight into clinical benefit requires demonstrating that TRPC6 inhibition can achieve meaningful preservation of kidney function in human patients over extended periods. The challenge lies in developing selective inhibitors that don't disrupt normal calcium signaling in other tissues. If successful, this approach could transform treatment for millions with chronic kidney disease by targeting the cellular machinery that maintains the kidney's filtration barrier.