Furthermore, TCF4 overexpression in ECs of heart failure patients increases their proliferation rate (Fig. 6G), and up-regulates their EC-specific functions, such as enhanced eNOS gene expression (Fig. 6H), increased NO production (Fig. 6I), and promotion of angiogenesis (as indicated by tube formation assay in Fig. 6J–L). This evidence concerns the gene NOS3 and heart failure.