In other words, the mechanism underlying the relative resistance of BM-NPC cells to be enhanced to secrete IL-6 in a much higher magnitude like P-NPC cells is possibly due to the insensitivity to the ongoing cooperation of IRF-1 and the p65 subunit of NK-κB for IL-6 activation at the level of IL-6 promoter by IFN-γ [45]. This evidence concerns the gene IRF1 and nasopharyngeal carcinoma.