FXR expression is decreased in NASH patients [25], which can aggravate the development of steatosis and NASH: (1) FXR activation represses hepatic lipogenesis via the FXR–SHP–SREBP1c pathway (see below for more on small heterodimer partner [SHP]), (2) FXR activation promotes β-oxidation by stimulating the expression of PPARα and CPT1, and (3) FXR activation reduces hepatic FA uptake by reducing the expression of CD36 [89]. Here, CD36 is linked to metabolic dysfunction-associated steatohepatitis.