In normal situations, the metabolism of triglycerides in the liver is regulated by insulin, which activates lipoprotein lipase (LPL), but in states of IR [25]—such as type 2 diabetes mellitus, metabolic syndrome, and obesity—insulin deficiency decreases LPL activity, which implies that there is a greater amount of free fatty acids in the blood that will allow greater synthesis of triglycerides in the liver, which will result in an excess of VLDL, which are particles that remain in the blood longer and thus increase their atherogenic power [26,27]. The gene discussed is LPL; the disease is metabolic syndrome.