The molecular interactions of modeled wild-type and mutant KLF4 with a 10-bp DNA sequence (5′-cgggcggggc-3′) in the P21CIP gene promoter, which is widely recognized as the transcriptional target site for KLF4 protein [18,19], revealed that T-ALL mutant KLF4 was unable to interact with its target DNA sequence as a result of mutation of the Zf3 motif, while wild-type KLF4 exhibited proper cation-π and hydrogen-bonding interactions with its target DNA sequence (Figure 4E). Here, KLF4 is linked to acute lymphoblastic leukemia.