Due to the essential role of EBF1 during B cell development, loss of EBF1 (16, 17) or an increase of one of its inhibitors [ZNF521 (18) or ZNF423 (19)] supports the development of B-cell acute lymphoblastic leukemia (B-ALL). The gene discussed is EBF1; the disease is precursor B-cell acute lymphoblastic leukemia.