Overexpression of miR-122 was shown to counteract lipid accumulation in cultured hepatocytes or in the liver of NASH mouse model through several mechanisms, such as: (i) Yin Yang 1, farnesoid X receptor, and small heterodimer partner (YY1/FXR/SHP) axis [140]; (ii) hypoxia-inducible factor-1alpha, vimentin, and mitogen-activated protein kinase kinase kinase 3 (HIF-1α/vimentin/MAP3K3) axis [141]; (iii) hepatocyte nuclear factor 4α (HNF4α) pathway [142]; stearoyl-CoA desaturase gene (SCD) [143]. This evidence concerns the gene HIF1A and metabolic dysfunction-associated steatohepatitis.