In this study, we generated and analyzed mice that lack PLCδ1 and PLCδ3 with extra-embryonic PLCδ1 expression and found that the simultaneous loss of PLCδ1 and PLCδ3 results in DCM-like phenotypes that are associated with excessive apoptosis of cardiomyocytes. The gene discussed is PLCD1; the disease is familial dilated cardiomyopathy.