Meanwhile, it is well known that the reprogramming of X-inactivation during acquisition of pluripotency is accompanied by the repression of XIST, the trigger of X-inactivation, and the upregulation of its antisense counterpart TSIX. Our data demonstrated that TSIX showed some correlation with FMR1-AS1 and overexpressed in CD44high ESCC cells and samples, indicating that sXCI within ESCC development may tend to the FMR1-AS1 highly expressed cells to contribute female ESCC tumorigenesis and malignancy. This evidence concerns the gene TSIX and esophageal squamous cell carcinoma.