Due to its well documented pro-catecholaminergic effects, it seems that the pharmacological inhibition of FFAR3 with a synthetic FFAR3-selective antagonist or with ketogenic drugs (e.g., SGLT2 inhibitors) that increase levels of ketone bodies (e.g., 3-hydroxybutyrate), FFAs that act as natural, endogenous FFAR3 antagonists, has the potential to treat several cardiovascular diseases aggravated by sympathetic nervous system hyperactivity, such as chronic heart failure, hypertension, coronary artery disease, atrial fibrillation, etc. However, there are some caveats to this premise. The gene discussed is SLC5A2; the disease is atrial fibrillation.