Therefore, the addition of FGFR-TKIs to ALK-TKIs can suppress the reactivation of cell survival signaling molecules through activation of FGFR1 kinase by binding FGFR1 and FGF2 proteins in FGFR1high and FGF2high ALK + NSCLC cells. This evidence concerns the gene FGF2 and non-small cell lung carcinoma.