Interestingly, intestine-specific disruption of PPARα and FABP1 in mice (196) suggests that intestinal PPARα signaling promotes nonalcoholic steatohepatitis (NASH) via the modulation of intestinal FABP1, which regulates dietary FA uptake, highlighting the potential importance of intestinal PPARα and FABP1 as targets for the treatment of NASH. This evidence concerns the gene FABP1 and metabolic dysfunction-associated steatohepatitis.