The above data illuminated that 9za was indeed a dual MEK/PDK1 inhibitor, and the dual suppression of the MEK/ERK and PDK1/Akt signaling axes strengthened the cytotoxicity and cell apoptosis compared with the single inhibition of the MEK or PDK1 signaling pathway in NSCLC cells. The gene discussed is PDK1; the disease is non-small cell lung carcinoma.