We predict that abnormalities in Ca2 + channels and dysregulation of Ca2 +-cycling proteins induce a sustained expression of cardiac fetal gene MYH6 and MYH7 which can then cause cardiac dysfunctions, hypertrophy and heart failure that have been linked to alterations in ECC, arrhythmia and cardiomyopathy. The gene discussed is MYH6; the disease is cardiac arrhythmia.