Molecular docking experiments, performed to assess the molecular mechanism of GQZ in the treatment of NSCLC, found that quercetin bound to AKT1, C-MYC and TP53, with highest affinity binding to AKT1, indicating that AKT1 may be the key target of the anti-NSCLC effect of GQZ. This evidence concerns the gene MYC and non-small cell lung carcinoma.