Furthermore, diacylglycerol o-acyltransferase 2 (DGAT2) and not PLIN5 appears to be the mediator in mitochondria segregation and ER-anchored lipogenic mitochondria generation [56], as demonstrated by the reduction on steatosis and hypertriglyceridemia upon DGAT2 ablation [57]. The gene discussed is DGAT2; the disease is steatosis.