Our results showed that prostate CAFs but not prostate cancer cells express a high level of CD63 and that prostate CAFs but not prostate cancer cells responded to TIMP-1 of or knockdown of TIMP-1 (Figures 6-7), suggesting that through CD63 receptor expressed by prostate CAFs, TIMP-1 can promote CAF proliferation and migration, which lead to accumulation of CAFs within cancer tissues. The gene discussed is CD63; the disease is prostate carcinoma.