In addition to genome-wide mutations, rearrangements, and accurate copy number (CN) changes our study incorporates EBV viral gene expression, revealing multiple important insights into NPC tumorigenesis further establishing the interrelated roles for both host somatic alterations and EBV gene expression impacting multiple cellular mechanisms, namely NF-κB activation, immune evasion, and persistent infection with EBV8–11,13,14. Here, NFKB1 is linked to nasopharyngeal carcinoma.