Taken together, our work identifies a previously undescribed function for the EphB6 receptor in controlling drug sensitivity of T-ALL cells and suggests that the efficiency of DNA-damaging therapeutic reagents, including doxorubicin, could be improved by applying them in a personalized manner to patients with different levels of EphB6 expression in T-ALL cells. The gene discussed is EPHB6; the disease is acute lymphoblastic leukemia.