On the other hand, Pillai et al. reported that cardiac-specific overexpression of Nampt induced cardiac hypertrophy and interstitial fibrosis spontaneously in mice, and that heterozygous knockout of Nampt attenuated isoproterenol- and angiotensin II-induced cardiac hypertrophy, indicating Nampt is a positive regulator of adverse cardiac remodeling9. The gene discussed is NAMPT; the disease is cardiac hypertrophy.