To date, there is no doubt that SEs acquired de novo are one of the hallmarks of esophageal carcinoma, and the available studies conclude the characteristics of the oncogenic SEs in esophageal carcinoma: (i) they are acquired based on genetic variants or TADs boundaries disruption, (ii) they drive the transcriptional additions depend on CRCs and convergence of tumorigenic signaling pathways, (iii) they could be targeted by inhibition of BRD4, CDK7, and histone acetylation, which exceptionally enriched within these cis-elements. The gene discussed is CDK7; the disease is carcinoma of esophagus.