Although we showed the therapeutic possibility of targeting the YAP/TEAD1 pathway by administration of TT-10 for LMNA-related DCM, previous studies raised the concern that overactivation of the YAP/TEAD1 pathway may induce cardiac dysfunction possibly because of CM dedifferentiation (34, 35). This evidence concerns the gene TEAD1 and familial dilated cardiomyopathy.