Our model presented hepatic steatosis and fibrosis, as previously described, and an inflammatory condition, which we demonstrated through of increase in the macrophage activity by the F4/80 marker, by the increase in the gene expression of F4/80 and pro-cytokines (IL-1B and TNF-α), in addition to increased activity of the IKKB protein, proteins of the inflammatory pathway. The gene discussed is IKBKB; the disease is fatty liver disease.