Thus, the novel findings presented herein that C10 can reverse HF diet-induced hepatic steatosis, glucose intolerance, as well as hepatic and visceral adipose inflammation, coupled with the finding that C10 inhibits Tnfa-induced Vcam1 expression and reduces monocytic cell adhesion to endothelial cells (Dagia et al. 2004), an important process in the pathogenesis of atherosclerosis and other chronic inflammatory diseases, suggests that C10 may have a more profound clinical impact than the treatment of NAFLD alone. The gene discussed is TNF; the disease is atherosclerosis.