We demonstrated that CD1a x CD3ε could represent an effective anti-T-ALL agent to be investigated in a first-in-human clinical trial as maintenance treatment, such as blinatumomab, for purging the minimal residual disease (MRD) or in CD1a-expressing refractory/relapsed patients to improve the poor disease control obtained with nelarabine. Here, CD1A is linked to acute lymphoblastic leukemia.