In human B cell acute lymphoblastic leukemia (B-ALL), which is the most common cancer in children, Pax5 is a haploinsufficient tumor suppressor, and the deletion of one Pax5 allele in mice cooperates with oncogenic mutations and with heterozygosity of the transcription factor Ebf1 to drive malignant transformation8–11. This evidence concerns the gene PAX5 and B-cell acute lymphoblastic leukemia.