These differences could indicate that a beneficial effect of spironolactone on APCs and PVCs is dependent on pathological processes that are less prevalent in HD patients than in congestive heart failure and ischemic heart disease, or that the effect requires a more extensive renin–angiotensin–aldosterone system inhibition, achieved through concomitant angiotensin-converting enzyme inhibitors treatment. The gene discussed is ACE; the disease is Huntington disease.