Furthermore, B-Myb depletion could suppress the activation of ERK and Akt signaling pathways though upregulation of IGFBP3 in NSCLC, and B-Myb overexpression could promote the activation of ERK and Akt signaling pathways through inhibition of IGFBP3. In conclusion, our present study demonstrated for the first time that B-Myb is an independent prognostic marker and serves as a potential target in the diagnosis and/or treatment of NSCLC, and that B-Myb functions as a tumor-promoting gene by targeting IGFBP3 in NSCLC cells. The gene discussed is AKT1; the disease is neoplasm.