KLF4 and acute lymphoblastic leukemia: Transfected control cells displayed increased transcriptional activity of the reporter construct containing the P21CIP promoter compared with T-lymphoblasts (Figure 4I), suggesting that mutant KLF4 protein in T-ALL loses its ability to bind to the KLF4-binding site present in the P21CIP promoter, and is thus unable to induce P21CIP.