Since GSK3 is a well-known substrate of Akt, it is likely that osimertinib inhibits Akt-dependent GSK3 phosphorylation in EGFRm NSCLC cells, leading to GSK3 activation and subsequent GSK3-dependent and FBXW7-mediated degradation of Topo IIα. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.