In light of the central role of the GK–GKRP complex in glucose homoeostasis and its subsequent causal involvement in the pathogenesis of T2D (Type 2 diabetes), hypoglycaemia and hypertriglyceridaemia, it is not surprising that intensive efforts have been directed towards developing pharmacological agents that target both proteins [3,14–16,18–21,22,34]. This evidence concerns the gene GCKR and hypertriglyceridemia.