Since most EBER signals presented the peritumor microenvironment in our patients, we presumed that EBERs could induce the initial transformation of epithelial cells [45], and trigger cancer-related inflammation via the RIG-I pathway to promote tumor development and growth [46]; rather than downregulate B2M expression to evade T cell-mediated cytotoxic immune responses [47], as according to previous NPC studies. The gene discussed is B2M; the disease is neoplasm.