GSK3β phosphorylates the Ser/Thr residues at the N-terminal of β-catenin, leading to the degradation of β-catenin.167 Huang et al.168 found that miR‐150 directly inhibited GSK3β expression at the protein level, resulting in the abnormal accumulation of β-catenin, leading to radiotherapy resistance of NPC cells. Here, GSK3B is linked to nasopharyngeal carcinoma.