further validated an interconnected circuitry formed by four master TFs‐ELF3, KLF5, GATA6, and EHF, which promoted each other's expression by interacting with each SE in esophageal cancer.[27] Moreover, SE activation drives KLF5 overexpression and promotes basal‐like breast cancer (BLBC) progression. The gene discussed is EHF; the disease is breast carcinoma.