The SL/Kh strain of mice develops spontaneous pre-B-ALL at more than 90% incidence by 6 months of age due to constitutive activation of STAT5a by retrovirus integration[9] and transgenic overexpression of STAT5aS711F cooperates with p53 deficiency to promote B-ALL [10]. This evidence concerns the gene TP53 and acute lymphoblastic leukemia.