We now consider that endogenous stem cell activity could correspond to specific pathophysiological myocardial changes that occur in the setting of cardiac pressure overload; initially an increased metabolic requirement correlates with an angiogenic response (EPC and SSEA1+ cells), and later, as heart failure and dysfunction becomes evident and cardiac myocyte apoptosis begins, the CSC population gets activated [44]. This evidence concerns the gene FUT4 and heart failure.