In the 2000s, imatinib mesylate (IM), a first-generation TKI, is quite efficient in apoptosis induction in CML stem cells by lowering programmed death receptor 1 (PD-1) expression on CD8+ T cells and monocytic myeloid-derived suppressor cells (MDSCs), resulting in increased cytotoxicity mediated by cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells; however, in another study it showed the enhanced expression of ATG4B and survival in CD34+ CML cells [158, 159]. The gene discussed is CD8A; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.