[5,53–56] Previous reports found CASZ1 damaging variants associated with VSD, DCM and LVNC, [18–20] consistent with studies of Casz1 constitutive and conditional knockout mice that showed reduced proliferation of embryonic cardiomyocytes, resulting in VSD and abnormally thin ventricular walls. The gene discussed is CASZ1; the disease is ventricular septal defect.