These data demonstrate that FGF21 inhibits the activation of ResKCs and MoKCs and prevents the accumulation of CD36hi ResKCs and CD36hi/CD9hi MoKCs under dietary conditions that result in NASH, which likely contribute to the beneficial effects of FGF21 on hepatic inflammation and fibrosis. This evidence concerns the gene FGF21 and metabolic dysfunction-associated steatohepatitis.