It has been reported that the decreased expression of PTEN, post-IR, induces radioresistance through promotion of cell proliferation and inhibition of cell apoptosis in non-small cell lung cancer and nasopharyngeal carcinoma.[13, 14] Directly restoring PTEN function has previously been reported to be a valuable approach to achieve radiosensitization in vitro.[15] However, whether PTEN participates in radiation-triggered EMT and tumor metastasis in ESCCs is not yet clear. This evidence concerns the gene PTEN and nasopharyngeal carcinoma.