KLF5 and cancer: Because CCAT1 expression was decreased in the deletion mutants of the KLF5 enhancer, it is suggested that the KLF5 enhancer may play a crucial role in the maintenance of cancer stemness by regulating KLF5 and CCAT1. Taken together, these results show that targeting therapeutics against the KLF5 enhancer, e.g., blockade of KLF5 promoter–enhancer binding by the decoy oligonucleotide strategy may be an efficient therapeutic option for CSCs.