We have previously shown an essential role for MCL-1L upregulation in the anti-apoptotic effect of IFNγ on imatinib treated JURL-MK1 cells.13 In line with this observation, IFNγ strongly upregulated MCL-1L expression and completely inhibited the pro-apoptotic effect of imatinib in primary human CD34+ CML stem/progenitor cells (Figure 6). Here, MCL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.