It has been reported that CASP8 facilitates the EMT process through enhancing the activity of Src,41 whereas blockage or mutation of CASP8 results in the escape of tumor cells from immune attack.30,42 Additionally, alterations in four driver genes (CDKN2A, BRAF, ERBB3 and TRAF2) that are significantly associated with ECI have already been described to serve essential roles in regulating apoptosis.43–45. The gene discussed is TRAF2; the disease is neoplasm.