Of note, a recent small, but well‐designed, study showed that administration of the GLP‐1 analog, liraglutide, led to histological resolution of NASH in a significant proportion of subjects.88 Moreover, the drug also reduced insulin resistance and decreased hepatic de novo lipogenesis and lipotoxicity in key metabolic organs.89 Thus, the ability of BA‐based therapies to augment GLP signaling warrants further investigation as part of understanding their potential as a disease‐modifying intervention in NASH. The gene discussed is INS; the disease is metabolic dysfunction-associated steatohepatitis.