A‐type natriuretic peptide (ANP) and B‐type natriuretic peptide (BNP) are secreted by the heart in response to increased wall stress, and these peptides promote vasodilation (reducing LV wall stress), stimulate renal sodium and water excretion (i.e. antagonizing the retention of salt and water characterizing HF), and inhibit pathological growth, that is, hypertrophy and fibrosis (key components of the adverse LV remodelling that occurs after MI and in HFrEF).19 The gene discussed is NPPA; the disease is hydrops fetalis.