TAFAZZIN and cardiomyopathy: AAV9-TAZ therapy administered to neonatal Taz KO mice was able to improve survival, reduce fibrosis, LV dilation and delay onset of cardiomyopathy when under the control of a CMV promoter but not a cardiomyocyte-restricted cTNT promoter, suggesting that the replacement of Tafazzin activity in skeletal muscle improves survival.