Several studies demonstrate that a quiescent population of CML stem cells (CD34+CD38–CD45RA–CD71–HLA–DRlow) with Bcr-Abl kinase domain mutations, detectable prior to initiation of imatinib therapy, gives rise to leukemia cells that persist because they are inherently resistant to imatinib (Sorel et al., 2004; Molofsky et al., 2005; Barnes and Melo, 2006; Jiang et al., 2007; Jorgensen et al., 2007; Niemann et al., 2007; Wodarz, 2008; Olsson et al., 2014). This evidence concerns the gene CD38 and chronic myelogenous leukemia, BCR-ABL1 positive.