To confirm the bioinformatics result suggesting that mutant KLF4 was unable to interact with its 10-bp target sequence in the P21CIP gene promoter in pediatric T-ALL, we transfected a β-galactosidase (β-gal) construct under the control of the P21CIP promoter and harboring a KLF4 site into control and T-lymphoblasts and subsequently incubated for 72 h at 37°C in humidified 5% CO2 atmosphere. The gene discussed is KLF4; the disease is acute lymphoblastic leukemia.