In summary, HFSD, fatty acid type, hyperleptinemia, microbiota overgrowth (and its consequent metabolites), and LPS, were able to enhance the production of the inflammatory biomarkers IL-6 and TNF-α; this induced and aggravated hepatosteatosis, thus allowing for progression toward different degrees of fibrosis in the experimental animals. The gene discussed is IL6; the disease is fibrosis.