In recent years, a variety of strategies and drugs have been developed to reverse the immunophenotype of TME: these include inhibition of Rho-kinase and FAK-mediated cell contraction (e.g., Fasudi, H1152, Defactintb), reduction of matrix components (e.g., FAP gene-editing cells, FAP-vaccine, FAP antibody-nanoparticle, VS-4718, and PEGPH20), inhibition of matrix cross-linking (e.g., BAPN and miRNA LOX inhibitors) and fibrosis (e.g., pirfenidone, losartan, and tranilast), improvement of tumor vascular leakage (e.g., bevacizumab), and reduction of the effect of vascular shear stress (2, 6, 7). This evidence concerns the gene FAP and neoplasm.