Notably, the pharmacological inhibition of NOX enzymes with apocynin reduces myocardial ROS production and diastolic dysfunction in rodent models of diabetes mellitus [82,83] and AngII infusion [84], as well as attenuating cardiac hypertrophy, fibrotic remodeling, and oxidative stress in response to AngII or aldosterone [84,85] and myocardial infarction injury [86], underscoring the centrality of NOXs to diastolic impairment and the deterioration of cardiac function in response to bolstered RAAS activity and comorbid cardiovascular disease. The gene discussed is AGT; the disease is cardiac hypertrophy.