It has been demonstrated that BCL11B is a haplo-insufficient tumor suppressor which collaborates with all major T-cell, acute lymphoblastic leukemia (T-ALL) oncogenic lesions during human thymocyte transformation[19], the loss of a BCL11B allele provides susceptibility to mouse thymic lymphoma[20] and human T-ALL[21-23]. This evidence concerns the gene BCL11B and acute lymphoblastic leukemia.