APOE ɛ2 is a known mediator of hyperlipidaemia, because of its inaccurate binding to LDL receptors, and can in the presence of other environmental factors increase the risk of atherosclerosis [9], which could be an explanation of the observed interaction effect in that this provides a synergistic detrimental effect with HbA1c on the vascular system with a downstream effect on attention/executive function. The gene discussed is LDLR; the disease is hyperlipidemia.