 A recent study using a conditional knockout mouse that either lacked beta-catenin altogether or expressed a non-degradable form of beta-catenin in cardiomyocytes reconciled a potential reason for these discrepancies.There appears to be strict control over the subcellular localization of beta-catenin in cardiac muscle.Mice lacking beta-catenin had no overt phenotype in the left ventricular myocardium; however, mice harboring a stabilized form of beta-catenin developed dilated cardiomyopathy, suggesting that the temporal regulation of beta-catenin by protein degradation mechanisms is critical for normal functioning of beta-catenin in cardiac cells.