In hypoxic BMM, there are increased levels of hypoxia-inducible factors (HIFs), being essential for regulation of proliferation, quiescence, TKI resistance, and survival of CML LSCs, as well as increased capacity of HSCs to transform into LSCs, mediated by increased glycolytic flux via glucose transporter 1 (GLUT1) and tumor M2-pyruvate kinase (PKM2), overexpression of P21, suppression of P53, increased transcription of antioxidant factors (FOXO and NRF2), and uptake of c-MYC [91–93]. The gene discussed is TP53; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.