Current mechanistic studies of pLELC primarily focus on genomic and transcriptomic profiles, revealing similarities to nasopharyngeal carcinoma (NPC)—including driver mutations in NF-κB, CDKN2A, and JAK/STAT pathways, analogous regulation of p53 and PD-L1, and shared type II latency features evidenced by LMP1/LMP2 expression (15, 41). This evidence concerns the gene SOAT1 and nasopharyngeal carcinoma.