Inactivation of phosphatase and tensin homolog deleted from chromosome 10 (PTEN), which is common in prostate cancer, increases acetylation of KLF5 through phosphorylated AKT (p-AKT) activation, which stimulates inflammatory cancer-associated fibroblasts (iCAFs) through TNF-α to release FGF9, which in turn activated FGFR1 signaling in prostate cancer cells. Here, FGF9 is linked to prostate carcinoma.