Furthermore, hyperglycemia, ROS, and inflammatory cytokines mediate hepatic steatosis by uncontrolled stimulation of the lipogenic transcription factors SREBP1/2 and their target CHOL, as well as TGs synthesis genes, and concomitant suppression of PPARα, which is responsible for the mitochondrial FAs (β)-oxidation [65]. The gene discussed is PPARA; the disease is Hepatic steatosis.