In summary, our results suggested that activation of the PI3K-AKT pathway in nasopharyngeal carcinoma cells might be the driver of acquired radiation resistance, which prompted us to further explore the relationship of the PI3K-AKT pathway in nasopharyngeal carcinoma cells, such as whether the phenotypic changes are caused by downstream mechanistic changes through protein-protein interactions (Figure S6), which will be further studied in the future. This evidence concerns the gene AKT1 and nasopharyngeal carcinoma.