CAFs could result from the activation of normal tissue-resident fibroblasts or transdifferentiated from non-fibroblastic lineage such as epithelial and endothelial cells following EMT and endothelial-to-mesenchymal transition in response to stimulations by cancer cells and/or other associated stromal cells (e.g., with transforming growth factor (TGF), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF) as key regulators) [57,58]. Here, EGF is linked to cancer.