Ex vivo Tead1 deletion in these neonatal cardiomyocytes mirrored the in vivo Tead1 deletion findings of up-regulation of α-skeletal actin (Acta1) and a down-regulation of both α-, β-MyHC (Myh6, Myh7) (Fig 4B), suggesting Tead1 regulation of these fetal program genes [15] in cardiomyocyte is unique and cell-autonomous and that tead1 is required for β-MyHC upregulation in heart failure. Here, MYH7 is linked to heart failure.