A study of embryonic day (E) 11.5 mouse hearts showed that the endocardial-specific deletion of Hand2 disrupted multiple endocardial signalling pathways and marker gene expression and caused congenital defects, including tricuspid atresia, double inlet left ventricle, and interventricular septal defects, suggesting that endocardial Hand2 is required for cardiac morphogenesis [39]. Here, HAND2 is linked to tricuspid atresia.