As indicated below, NAFLD may be associated with a decrease in muscle mass as a consequence of (i) insulin-resistance, (ii) decreased IGF-1 production by the liver, (iii) decreased AA flows to the muscles due to increased splanchnic utilization, (iv) a defective postprandial peripheral vasodilatory response, or (v) the catabolic effect of various mediators, including hepatokines, produced by the liver in steatosis-induced situations of endoplasmic reticulum (ER) stress. The gene discussed is IGF1; the disease is steatosis.