Interestingly, following up the seminal work by Luo et al. and Vasiri et al. [6,7], a very recent study by Li and coworkers [42] explored the Sirt1-p53 axis in chronic myeloid leukemia (CML) and found that targeting of Sirt1 by either shRNA or the small molecule inhibitor tenovin-6 resulted in increased levels of acetylated p53 in CML CD34+ cells accompanied by increased transcriptional activity of p53. The gene discussed is CD34; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.