Notably, the mesenchymal components of TME amplify the drug resistance effect through bidirectional interactions: CAFs induce the expression of multidrug-resistant proteins through the secretion of cytokines HGF and FGF; whereas aberrantly functioning tumour vascular endothelial cells (TECs) promote self-renewal of tumour stem cells through factors such as VEGF to form a subpopulation of cells with high drug resistance subpopulation of cells with high drug resistance potential [98]. Here, HGF is linked to neoplasm.