RAC1 and chronic kidney disease: In the kidney, Rac1 is shown to act as a regulatory subunit of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, and the resultant ROS exert proinflammatory responses via NF-κB activation.[23, 24] We previously reported that Rac1 inhibitors conferred renoprotection, in part by suppressing inflammatory signals in several chronic kidney disease models.[25–28].