ALT TRPC6-mediated podocyte injury and mechanism of action of BI 764198 in FSGS. TRPC6 overactivation, triggered by immune-mediated injury, maladaptive hemodynamic stress, or gain-of-function mutations, leads to excess intracellular calcium influx in podocytes. This activates calcineurin/NFAT and RhoA-dependent signaling, resulting in downregulation of critical slit diaphragm proteins including nephrin and synaptopodin, foot process effacement, and proteinuria. BI 764198 selectively inhibits TRPC6, interrupting this cascade at the channel level. Abbreviations: TRPC6, transient receptor potential cation channel, subfamily C, member 6; NFAT, Nuclear factor of activated T-cells; RhoA, Ras homolog family member A. Created with BioRender.com.