The ANP/NPR-A interaction oversees the control of myocardial hypertrophy as the scientific literature has extensively documented; the BNP/NPR-A interaction regulates the mechanism of fibrosis: deletion of the BNP gene results in normal pressure values and regular cardiac volumes in mice, but can also generate ventricular fibrosis especially if the animal has received pressure overload [120]. The gene discussed is NPPB; the disease is cardiac hypertrophy.