This is exemplified by the observation that the inactivation of PRDM16 in WAT and BAT resulted in the development of obesity, severe insulin resistance, and hepatic steatosis, and the investigators demonstrated that these phenotypes linked to a dramatic reduction in the browning of WAT, and thereby a significant reduction in energy expenditure [40]. The gene discussed is PRDM16; the disease is obesity due to melanocortin 4 receptor deficiency.