CASP8AP2 and acute lymphoblastic leukemia: In the present study, we showed that E2F3a could activate CASP8AP2 transcription directly; its over-expression enhanced the sensitivity of leukemic cells to chemotherapeutic drugs, and could be counteracted by knock down of CASP8AP2. Thus, in childhood ALL, the prognostic significance of E2F3a was largely implemented through regulating CASP8AP2 expression.