These mice have a normal life span and do not develop malignancies.30 The hypothesis of the oncogene function of BCL11B is further supported by research of our group, showing that BCL11B is overexpressed in the majority of T-cell acute lymphoblastic leukemia (T-ALL),21 and inhibition of BCL11B using siRNA leads to apoptosis of malignant but not normal T cells.31 This indicates that malignant T cells need BCL11B for their survival. This evidence concerns the gene BCL11B and T-cell acute lymphoblastic leukemia.