In esophageal cancer research, Klf5 has been shown to promote ESCC transformation by regulating Sox2 binding sites—specifically, it physically interacts with Sox2, guides Sox2 to newly opened chromatin regions and de novo super-enhancers (which drive the expression of oncogenes such as STAT3), stabilizes Sox2’s binding to these de novo sites, and forms a positive feedback loop with Sox2 (where Sox2 activates Klf5 transcription, and Klf5 in turn reinforces Sox2’s oncogenic binding activity). The gene discussed is SOX2; the disease is esophageal cancer.