In TAC-operated mice, FK866 treatment induced a significant decrease in myocardial concentration of NAD+ (Fig. 4b) and deacetylase activity of Sirt1 (Fig. 4c), and an increase in acetylation level of FoxO1 (Fig. 4d), although these changes were not observed in sham-operated mice (Fig. 4b–d). The gene discussed is SIRT1; the disease is persistent truncus arteriosus.