Mechanistically, SIMALR binds to eEF1A2 (eukaryotic translation elongation factor 1 alpha 2), and enhances its endogenous GTPase activity, thereby accelerating protein synthesis; it further promotes eEF1A2 phosphorylation, which in turn facilitates the translation of ITGB4/ITGA6 to drive the malignant phenotype of NPC cells [71]. This evidence concerns the gene EEF1A2 and nasopharyngeal carcinoma.