As we could observed, RASSF1A has an endogenous ability to promote apoptosis in CNE-2 cells, however, this activity is indeed dramatically stimulated by activated K-Ras in nasopharyngeal carcinoma cell lines CNE-2, which is contrast to the observations by Shivakumar et al in mammary adenocarcinoma cells[27]. Here, KRAS is linked to nasopharyngeal carcinoma.