Deficient CPT1A expression in the liver results in a healthy steatotic state that protects against high-fat diet-induced liver damage and increases adipose browning in a PPARα-FGF21 axis dependent manner, suggesting that inhibition of hepatic CPT1A may serve as a viable strategy for the treatment of obesity and NAFLD (Weber et al., 2020; Sun et al., 2021). The gene discussed is CPT1A; the disease is obesity due to melanocortin 4 receptor deficiency.