These findings suggest that cell survival against ALK-TKIs is activated by FGFR1 signaling involving AKT or ERK phosphorylation in FGFRhigh and FGF2high ALK + NSCLC cells, and the FGFR1 and FGF2 proteins promote escape from ALK-TKI-induced cell death. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.