The relationship between CAF and other components of the TME, such as inflammatory cells and vessels, is very complex, and it is mediated by a series of growth factors [vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF)], TGFβ, cytokines, and chemokines [monocyte chemoattractant protein (MCP-1) and C-X-C motif ligand (CXCL) 12 and 14] and MMPs that promote tumor growth and spread, modifying the matrix, attracting the precursors of vascular and lymphatic vascular cells, and favoring an immunosuppressive microenvironment[15]. This evidence concerns the gene TGFB1 and neoplasm.