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. The gene discussed is NFKB1; the disease is hyperlipidemia.