In addition to the paracrine crosstalk between cancer cells and CAFs, FGF9 was more potent in activating FGFR1 signaling in prostate cancer cells with the KLF5KR mutant (Figure 5G), suggesting that the overactivated FGFR1 signaling caused by KLF5KR knockin could be attributed to additional endogenous molecular mechanisms in cancer cells. The gene discussed is FGFR1; the disease is prostate cancer.