Tumors classified under PTCL-EBV exhibited significantly shorter median OS (4.6 months versus 14.7 months in NKTCL, p = 0.001), and PD-L1 was also identified to be significantly upregulated in PTCL-EBV likely from upstream pathways such as NK-κB and IFNγ which induce PD-L1 expression, presenting a potential biomarker for targeted therapy. This evidence concerns the gene CD274 and extranodal nasal NK/T cell lymphoma.