Notably, in the absence of cytokines, TKI treatment was shown to downregulate the expression of BCL-xL [13, 14] as well as several other antiapoptotic members of the BCL2 and baculoviral IAP repeat containing (BIRC) gene families in CML cells [14] leading us to analyze whether the addition of a small-molecule MCL1 inhibitor such as S63845 might enhances the antitumorigenic effects of TKIs on CML cells. This evidence concerns the gene BCL2 and chronic myelogenous leukemia, BCR-ABL1 positive.