Insulin resistance was shown to increase free fatty acids availability, while hyperinsulinemia and hyperglycaemia promote triglyceride synthesis via the activation of carbohydrate-responsive element-binding protein (ChREBP) [65] and sterol regulatory element-binding transcription factor 1 (SREBF1c) [66], respectively and the consequent increase in cholesteryl ester transfer protein (CETP) activation. The gene discussed is MLXIPL; the disease is hyperinsulinism.