Our results suggest that DON action can be divided into two sequential steps (1) an initial phase occurring within the first 3 h after administration where DON induced an increased insulin, adrenaline and corticosterone release, a rise in liver lipogenesis and adipose tissue lipolysis associated with inflammation and ER stress; and (2) a second subsequent phase (6–12 h) where despite normalization of insulinemia and inflammation, the increased blood NEFAs and TG resulting from adipose lipolysis drives liver steatosis, a steatosis amplified by the drop in liver beta oxidation and lipolysis. The gene discussed is INS; the disease is steatosis.