NKX2-5 and ventricular septal defect: Moreover, mild VSD was detected in 37.5% of HE mice and 20% of cardiomyocyte‐specific knockout mice (crossing Wdr62‐floxed mice to Nkx2.5‐Cre mice to generate Wdr62fl/fl or fl/+; Nkx2.5‐Cre) (Figures 2H–J) Taken together, knocking out Wdr62 caused not only TOF phenotypes, but also other defects associated with malformation of RV and OFT, especially VSD.