Moreover, the deletion of ALCAT1 or pharmacological inhibition of ALCAT1 in mice has been shown to reduce high-fat-diet-induced obesity and insulin resistance, attenuate hepatic lipogenesis and fibrosis, and thus prevent the onset of diet-induced nonalcoholic fatty liver diseases [33,123]. The gene discussed is LCLAT1; the disease is metabolic dysfunction-associated steatotic liver disease.