This NAFLD phenotype is partly a consequence of miR-122 target genes upregulation, but it is also the result of alterations in lipid secretion, increased lipogenesis, tumor necrosis factor alpha (TNF-α), elevation of chemokine (C-C motif) ligand 2 (CCL2), interleukin 6 (IL-6) and macrophage recruitment [179,180]. Here, TNF is linked to metabolic dysfunction-associated steatotic liver disease.