Increases in miR-29a cause downregulation of tumor suppressor TET2 and antioxidant-coding EPAS1, as well as overexpression of anti-apoptotic genes BCL-2 and MCL-1, resulting in greater TKI resistance in CML LSC [146, 147]. The gene discussed is BCL2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.