Although our findings conflict with a previous study in GPR35 knockout mice, existing evidence of pathological roles for Gα13/RhoA/ROCK signaling in the cardiovascular system, including prohypertensive and prohypertrophic effects, provide a rationale for why GPR35 knockout mice are protected from cardiovascular disease.26–28 More in-depth investigation of the activation of these components in GPR35 knockout models of cardiovascular disease may yield insights into potential mechanisms of Ang II–induced hypertension resistance in GPR35 knockout mice. The gene discussed is AGT; the disease is hypertensive disorder.