Furthermore, activation of mammalian rapamycin (mTOR) was attenuated and drug resistance increased in hypoxic T-ALL cells; meanwhile, HIF-1α KD also restored mTOR activity at hypoxic concentrations and suppression of mTOR in HIF-1α KD T-ALL impaired the chemotherapeutic effect in leukemic cells.94 The gene discussed is HIF1A; the disease is acute lymphoblastic leukemia.