Since it has been described that the accumulation of hepatic lipids—mainly diglycerides—contributes to altered insulin signaling that could trigger a rise in circulating glucose levels (Samuel and Shulman, 2016), it is tempting to speculate that the increased glycerophosphocholine and diglycerides observed in L18 rats could account for this hyperglycemia. The gene discussed is INS; the disease is Hyperglycemia.