These changes inhibited the expression of hepatic FXR signaling (CYP7A1 and FXR), thus triggering increased hepatic expression of pro-inflammatory cytokines (TNF-α and IL-6) [35] and hepatic lipid metabolism associated genes (SREBP-1c, FAS, and ACC) [24], leading to the unique characteristics of NAFLD. This evidence concerns the gene NR1H4 and metabolic dysfunction-associated steatotic liver disease.