Since, both Yap and Taz act as co-activators of Tead1, early neonatal death due to Yap/Taz combined deletion is consistent with our observation of early neonatal death secondary to heart failure with decreased cardiomyocyte proliferation after Tead1 deletion in cardiomyocytes, using the same Myh6-Cre line. Here, YAP1 is linked to heart failure.