Thus, it is conceivable that dysregulation of Gi/o signaling due to the absence of RGS2, RGS5, or both RGS proteins could also lead to the loss of homeostatic negative regulation or profibrotic CREB activation, predisposing to the disinhibition of sympathetic-mediated myocardial fibrosis in DCM. The gene discussed is RGS2; the disease is familial dilated cardiomyopathy.