Overexpressing wild type Nkx2.5 or one of its homeodomain (HD) mutants such as I183P in murine cardiomyocytes under the control of β-myosin heavy chain promoter resulted in embryonic lethality and/or heart failure, which was a consequence of dilated cardiomyopathy and/or a defective conduction system [7]. Here, NKX2-5 is linked to dilated cardiomyopathy.