LPL hydrolyzes triglyceride (TG) into fatty acid and glycerol (Bechmann et al. 2012) and hepatic lipase deficiency exhibited glucose intolerance and hepatic steatosis (Andres-Blasco et al. 2015), whereas increasing LPL rescued glucose and insulin tolerance in high fat diet-induced obesity (Walton et al. 2015). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.