AKT1 and non-small cell lung carcinoma: Having demonstrated the requirement for the AKT/mTOR signaling inhibition to achieve a down-regulation of glucose utilization and hence a better anti-proliferative response in NSCLC cells (see effects of dovitinib versus selective FGFR inhibitors in H1703 cells), we hypothesized that NVP-BGJ398 treatment might be conveniently associated with inhibitors of the PI3K/AKT/mTOR pathway in those cell models in which FGFR1 inhibition is not sufficient to inhibit this signaling cascade in the presence of serum.