Taken together, our data show that the interaction between GAS2 and CXCR4 promotes T‐cell leukemogenesis partially through NOTCH1/c‐MYC activity, whereas GAS2 impairment does not perturb the growth of normal hematopoietic cells, which demonstrates the critical role of GAS2 in T‐ALL pathology and potentiates GAS2 as a novel therapeutic target for this disease. The gene discussed is MYC; the disease is acute lymphoblastic leukemia.