Analogs of FGF21 that are able to maintain balanced and sustained agonism of FGFR1c, FGFR2c, and FGFR3c throughout the inter-dose interval appear to show the most promising pharmacological profiles, with among the largest reported decreases in liver fat of any therapeutic mechanism tested in NASH patients, and with encouraging signs of resolving NASH histology and fibrosis after relatively short-term treatment. The gene discussed is FGF21; the disease is metabolic dysfunction-associated steatohepatitis.