Although Hsp16.2 has been shown to inhibit cell death by binding to Hsp90, and through the activation of the PI-3kinase/Akt pathway [30] and was also been found to be overexpressed in esophageal cancer [62], the intensity of the Hsp 16.2 staining showed no significant relationship with either the time to metastasis or 10-year OS in our present study. Here, AKT1 is linked to esophageal cancer.