Interestingly, Ph+ B-ALL cells displayed the highest sensitivity to 2-DG and ER-stressors (i.e., either tunicamycin or thapsigargin), as these compounds translationally repressed prosurvival Myeloid cell leukemia 1 (Mcl-1) protein by activating the AMPK mechanistic target of rapamycin (mTOR) and UPR/PERK/eIF2α signaling pathways. The gene discussed is MTOR; the disease is acute lymphoblastic leukemia.