Similarly, another study highlighted that, in the nasopharynx carcinoma model, the EVs could package latent membrane protein 1 (LMP1) to transform normal fibroblasts into CAFs by virtue of the NF-κB P65 signaling cascade, and the activated CAFs were essential for promoting the proliferation and migration of nasopharyngeal carcinoma cells via aerobic glycolysis and autophagy. This evidence concerns the gene PDLIM7 and nasopharyngeal carcinoma.