Although CM1 cardiomyocytes did not appear to be substantially more proliferative than cardiomyocytes from other clusters that were present in injured and uninjured hearts through P42, they may have been primed for cell-cycle reactivation by the upregulation of regulatory molecules that contribute to cardiomyocyte proliferation (TBX5, TBX20, and ERBB4) and cardiac hypertrophy (GRK5). This evidence concerns the gene TBX5 and cardiac hypertrophy.