Besides, gliclazide and ramipril as constituents of our triple combination therapy, reduced mitochondrial superoxide generation, inhibited NADPH oxidase (NOX) via azabicyclo-octyl ring structure of gliclazide, leading to suppressed intercellular adhesion molecule-1 (ICAM-1; an inflammatory glycoprotein), reduced ROS-induced oxidative stress, myocardial fibrosis, cardiomyocyte apoptosis, cardiomyocyte hypertrophy, diastolic dysfunction, and enhanced production of SOD in experimental models of DCM and diabetic nephropathy (Onozato et al., 2004; Huynh et al., 2012; Pan et al., 2020). The gene discussed is FMO5; the disease is Myocardial fibrosis.