As known, normal resident tissue fibroblasts upregulate the expression of smooth muscle α-actin (α-SMA), the most common marker of myofibroblasts, and acquire a myofibroblast-like phenotype upon de novo activation by numerous soluble factors, such as the transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF) secreted from the neighboring tumor cells (Vonlaufen et al., 2008; Yin et al., 2013). Here, TGFB1 is linked to neoplasm.