Similarly, the cardiomyocyte-specific loss of Rac1, which is required for the induction of NOX2 oxidase activity, rescues diastolic dysfunction in response to pressure overload [94] and suppresses cardiac hypertrophy, fibrosis, and oxidative stress in response to AngII [61] and streptozotocin-induced diabetes [83]. The gene discussed is AGT; the disease is diabetes mellitus.