Zhang et al. [44] demonstrated this dual effect in impairment of hERG potassium channels (IKr) in vitro, proposing a depletion of ATP in hypoglycaemia impairs IKr function and an overproduction of reactive oxygen species (ROS) in hyperglycaemia impairs function of the same ion channel but by a different mechanism. The gene discussed is KCNH2; the disease is Hypoglycemia.