On the other hand, the increase in NPC cell viability induced by UPF1-KD was abolished by treatment with these inhibitors, suggesting that UPF1-KD promoted NPC cell growth through the activation of the p38/MAPK and JAK2/STAT3 pathways, which was mediated by the upregulation of COX-2 expression (Figure 5K, Supplementary Figure 5C). This evidence concerns the gene UPF1 and nasopharyngeal carcinoma.