The modulation of the renin-angiotensin-aldosterone (RAS) and sympathetic nervous systems through the use of angiotensin-converting enzyme inhibitors (ACE-i) or an angiotensin receptor-neprilysin inhibitors (ARNI), beta-blockers, and mineralocorticoid receptor antagonists (MRA) has been proven to enhance survival, lessen the risk of HF hospitalizations, and reduce symptoms in patients with HF [8–10]. The gene discussed is MME; the disease is hydrops fetalis.