Klf5 deficiency acted as an antioxidant, inhibited apoptotic transcriptional programs, including pro-apoptosis gene Fas, Tnfsf10, Irf7 and Casp4, and induced the anti-apoptosis gene Birc5, a finding opposite that to reported for Klf5 in other types of B-ALL [18]. The gene discussed is FAS; the disease is precursor B-cell acute lymphoblastic leukemia.