In addition to this upregulated miRs, Musumeci et al. demonstrated that miR-15 and miR-16 were downregulated in fibroblasts surrounding prostate tumor, and that such downregulation in CAFs promoted tumor growth and progression through the reduced post-transcriptional repression of FGF-2 and its receptor FGFR1, which act on both stromal and tumor cells to enhance cancer cell survival, proliferation, and migration [54]. The gene discussed is FGFR1; the disease is neoplasm.