Nonetheless, consistent with the single point Ser871Ala mutation, which only alters AMPK signalling to HMGCR rather than affecting AMPK's other functions such as those involved in glucose uptake or fatty acid synthesis, our results show that glucose homeostasis, serum proinflammatory cytokines and triglyceride levels were comparable between control and Apoe−/−/Hmgcr KI mice, confirming that increased atherogenesis in Apoe−/−/Hmgcr KI mice was unlikely to be due to hyperglycaemia, systemic inflammation or hypertriglyceridemia. The gene discussed is APOE; the disease is hypertriglyceridemia.