Modelling this subtype of B-ALL in mice has shown that animals conditionally expressing the E2A-PBX1 fusion oncogene develop B-ALL with a varied incidence from 5% to 50%, depending on the Cre recombinase (Cd19, Mb1, or Mx1) used to induce E2A-PBX1 expression [58]. The gene discussed is PBX1; the disease is precursor B-cell acute lymphoblastic leukemia.