Inversely, other experimental evidence obtained using different methodologies showed that the deletion of NPR-C in mice leads to basal atrial fibrosis and cardiac arrhythmias, as well as exacerbated AngII-induced atrial fibrosis [65,66], likely mediated by the less studied ability of NPR-C to activate inhibitory G proteins. The gene discussed is NPR3; the disease is cardiac arrhythmia.