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. Here, PAX5 is linked to precursor B-cell acute lymphoblastic leukemia.