These results demonstrated that GSK3β is not a substrate for SRPK1 and this was further confirmed by in vitro kinase assays (Fig. 4H, I), indicating that SRPK1 enhances GSK3β Ser9 autophosphorylation independently of its kinase activity, which may in turn increase resistance to gefitinib in NSCLC. This evidence concerns the gene GSK3B and non-small cell lung carcinoma.