Even more impressive, Lee et al. recently demonstrated that normalization of the NAD+ redox balance by NMN treatment or overexpression of the rate-limiting enzyme for NAD+ synthesis, nicotinamide phosphoribosyltransferase (Nampt), improved cardiac hypertrophy and dysfunction induced by isoproterenol treatment or TAC, strongly suggesting that NAD+ repletion may represent a promising therapeutic approach to treat cardiac hypertrophy and heart failure (82). This evidence concerns the gene NAMPT and cardiac hypertrophy.