Since Casp8−/− mice exhibit barrier defects, we speculate that in the carcinogen-induced tumor model, there is an increase in the penetration rate of 4NQO when compared with WT mice, which is consistent with our previous report in human OSCC lines that inactivating mutations in CASP8 promote OSCC growth in culture by reducing intercellular adhesion (3). This evidence concerns the gene CASP8 and neoplasm.