First, tumor cells harboring KRAS or NF-κB mutations release mitogenic and fibrogenic factors that can reprogram normal pro-fibrotic cells into active TAFs, including vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), TGF-β, and sonic hedgehog (SHH) [161–164]. This evidence concerns the gene VEGFA and neoplasm.