Although we showed the involvement of the former in mediating regression of cardiac hypertrophy after DeTAC here, at present, FoxO1-mediated upregulation of atrogin-1/MAFbx, a muscle-specific E3 ubiquitin ligase [12], and its involvement in regression of cardiac hypertrophy after DeTAC cannot be excluded. This evidence concerns the gene FBXO32 and cardiac hypertrophy.