As neprilysin is responsible for the degradation of atrial and brain natriuretic peptides, the cardiovascular and renal effects of sacubitril's active metabolite (LBQ657) in heart failure are attributed to the increased levels of peptides that are degraded by neprilysin (e.g., atrial natriuretic peptide), whereby its administration results in increased natriuresis and urine cyclic guanosine monophosphate (cGMP) and decreased plasma midregional pro atrial natriuretic peptide (MR-proANP) and N-terminal pro b-type natriuretic peptide (NT-proBNP). This evidence concerns the gene MME and heart failure.