The main reason for the failure of Bcl2 to hedge against PEITC-induced cell death may be that PEITC induces apoptosis in p53-mutant ESCC cells by the caspase pathway, and another reason may be that the relative level of BAX is higher than that of Bcl2, which results in an increases BAX homodimers thereby promoting cell death. This evidence concerns the gene BAX and esophageal squamous cell carcinoma.