More recently, Ebf1 haploinsufficiency resulting from the insertion of a lentiviral vector in its locus was reported to trigger the occurrence of B-ALL [48]. Ebf1 haploinsufficiency has also been linked to increased susceptibility of pro-B-cells to DNA damage in response to UV light and, though not highly leukaemogenic per se, induced pro-B-ALL development with high frequency when accompanied by Pax5 heterozygosity [49]. The gene discussed is PAX5; the disease is acute lymphoblastic leukemia.