Mice with activating SHP2 mutations in the endocardial cell lineage have increased proliferation of OFT endocardial cushion endothelial and mesenchymal cells, leading to cardiac malformations such as ventricular septal defects and DORV (Krenz et al., 2008; Combs and Yutzey, 2009). This evidence concerns the gene PTPN11 and ventricular septal defect.