Thus, mutations in E2a, Ebf1, Pax5, Runx1, Ras, Irf4, Irf-8 or Ikaros can be found in a large proportion of pediatric and progenitor leukemias [62]; however, model tumors show that leukemogenesis is more efficient by expressing constitutively active STAT5 (STAT5-CA) in combination with the loss of one allele of Ebf1 or Pax5 which induce a partial block in B cell differentiation. Here, STAT5B is linked to leukemia.