TEAD1 and heart failure: To confirm that these changes were primarily due to the cell-autonomous loss-of-function of Tead1, and not secondary (non-cell autonomous) changes from heart failure, we used our, previously described, ex vivo knockout model [11], wherein we compared gene expression changes with Tead1 deletion ex vivo, in Tead1F/F neonatal cardiomyocytes treated with Ad-Cre, as compared to that with control Ad-lacZ treatment.