Notably, KLC2 knockdown from CML cells promoted cell growth, decreased imatinib sensitivity (Fig. 2J–L), and reduced cleaved PARP-1 indicating that the imatinib-induced apoptosis in CML cells required KLC2 (Supplementary Fig. S6A,B). The gene discussed is KLC2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.