However, activation of FGFR with FGF autocrine signaling in specific FGFRhigh and FGFhigh cells, including FGFR1 with FGF2 or FGF9; FGFR2 with FGF2, FGF7 or FGF9; FGFR3 with FGF2 may have a compensatory role in promoting the survival and growth of DTP and resistant cells during treatment with targeted TKIs alone, and combined FGFR and targeted TKIs may be a promising therapeutic strategy to prevent a targeted TKI-induced DTP state or drug resistance against these specific FGFRhigh and FGFhigh cancer at baseline with various driver oncogenes. This evidence concerns the gene FGFR3 and cancer.