In NPC, O-GlcNAcylated HOXA9 enhances the expression of UBR5 and the ubiquitination and degradation of SIRT6, knockdown of HOXA9 or UBR5 promotes ferroptosis and inhibits NPC growth in mice, which provides a potential therapeutic target for NPC treatment [28]. This evidence concerns the gene SIRT6 and nasopharyngeal carcinoma.