Increased lipid influx into the liver or reduced lipid disposal precipitates hepatic steatosis, primarily instigated by a HFD, genetic predisposition, gut microbiota, and upregulated expression of lipid transcription factors (e.g, SREBP1c, chREBP, and PPAR-γ) [36]. This evidence concerns the gene SREBF1 and Hepatic steatosis.