Taken together, our findings demonstrate that STAT3 and NFκB may be critical mediators of the hyperlipidemia-related pathologies of atherosclerosis, NAFLD, obesity and type II diabetes/insulin resistance via miR-155, which being upregulated/present in mice having an atherosclerosis background, worsens atherosclerosis but does not significantly affect the health of the liver, adipose tissue, or blood glucose levels. Here, NFKB1 is linked to metabolic dysfunction-associated steatotic liver disease.