In this issue of Blood, Khorashad et al show that genetic (eg, short hairpin RNA [shRNA]-mediated) or pharmacologic (eg, KPT-330 [selinexor]) inhibition of nucleocytoplasmic protein trafficking restored sensitivity to tyrosine kinase inhibitors (TKIs) and impaired clonogenic potential of chronic myeloid leukemia (CML) cell lines with BCR-ABL1 kinase-independent TKI resistance (see figure).