Metabolic (hyperglycemia, dyslipidemia, ox-LDL, etc.)and non-metabolic stimuli (Ang II, aldosterone, vascular endothelial growth factor, etc.)activate the expression and activity of NADPH oxidases (Gill and Wilcox, 2006; Yang et al., 2020), resulting in ROS overproduction, which is involved in vascular, glomerular, renal tubular, and endothelial dysfunction, mesangial proliferation, and increase in renal sodium reabsorption, eventually resulting in hypertension and CKD (Wan et al., 2016; Ravarotto et al., 2018). This evidence concerns the gene FMO5 and metabolic syndrome.