In support of the aberrant role in hyperglycaemia, elevated expression of BRD4 was demonstrated in the myocardium of several preclinical models of DCM (STZ‐mice and rats and HFD‐mice), with pharmacological inhibition of BET activity (BET inhibitor, JQ1) leading to attenuation of pathological cardiac remodelling and subsequent improvements in cardiac function [94, 95, 96]. The gene discussed is DNER; the disease is familial dilated cardiomyopathy.