RGS11 is a regulator of G protein signaling that functions as a GTPase-activating protein (GAP), increasing the intrinsic GTPase activity of Gαi family subunits to drive them into their inactive GDP-bound state 1. RGS11 contains conserved DEP and GGL (G protein gamma-like) domains, with the GGL domain mediating interaction with Gβ5 to form functional complexes 2. Mechanistically, RGS11-Gβ5 complexes show differential selectivity among Gαi family members, with RGS11 exhibiting 2-4 fold higher maximal GAP activity compared to RGS7 and RGS9 1. In the retina, RGS11 and RGS7 work redundantly as GAPs in ON-bipolar cells, where R9AP stabilizes the RGS11-Gβ5 complex and accelerates light-response kinetics 34. Beyond vision, RGS11 has critical cardioprotective functions: it forms complexes with CaMKII and ATF3, counterbalancing oxidative stress and apoptosis triggered by chemotherapy 5. RGS11 downregulation in response to doxorubicin promotes cardiac fibrosis and dysfunction, while cardiac-specific RGS11 overexpression decreases chemotherapy-induced cardiotoxicity 5. Additionally, RGS11 modulates intercellular communication through regulation of cardiokine signaling, affecting hepatic injury following chemotherapy 6. RGS11 is a potential lung cancer biomarker with clinical implications for early diagnosis 7.