This is based on three lines of evidence; (i) FK866 increases the levels of acetylated p53, the functionally active form of p53, by inhibition of NAMPT/NAD+/SIRT pathway, (ii) by this mechanism FK866 increases expression of p21 and BAX, genes relevant in p53-mediated tumor suppressor functions and (iii) in the absence of functional p53, the effect of FK866 on leukemia cells is attenuated. The gene discussed is BAX; the disease is leukemia.