FGF19 and steatosis: MiR-181b and miR34a have been recognized to play crucial roles in steatosis development, acting as SIRT1 suppressors in case of palmitic acid exposure and both SIRT1 and PPAR suppressors in case of HFD exposure [114,115], as well as inhibiting β-Klotho, a co-receptor of the fibroblast growth factor 19 (FGF19), mainly involved in glucose metabolism, whose reduction was demonstrated related to inflammation, ballooning, and fibrosis [116].