This is the case of dyslipidemia, hyperglycemia, insulin resistance, and hypertension, which affect NOS activity through ROS formation increase mediated by several sources (NOXs and xanthine oxidase, dysregulated mitochondria, and uncoupled NOS) activated by FFAs, high glucose, AGE, angiotensin II, etc. Other intracellular pathways have been reported to alter •NO formation in MS by upregulating or downregulating the different NOS isoforms. This evidence concerns the gene NOS1 and Insulin resistance.