While, in the absence of drug resistance, TKIs are effective against the majority of CD34+CD38+ and CD34+CD38− cells in CML patients 14, 15, more primitive LSCs are much less susceptible to the apoptosis induced by TKI treatment, with their persistence maintaining disease 16, 17, 18, 19. This evidence concerns the gene CD38 and chronic myelogenous leukemia, BCR-ABL1 positive.