Converging evidence from human and pre-clinical mouse studies indicate that, as DCM progresses to HF Stages C and D, the protective action of the corin-ANP-cGMP axis is impaired as the coordinated relationship between cardiac pro-ANP expression and enzymes responsible for pro-ANP activation (corin) and ANP degradation (neprilysin) become imbalanced. This evidence concerns the gene MME and familial dilated cardiomyopathy.