In this setting, BRAF inhibitor reprograms CAFs by enhancing platelet-derived growth factor receptor (PDGFR) activity, thus increasing ECM production –thrombospondin (THBS)-1/2, tenascin C (TNC), or POSTN, among other matrix components– and stiffness to potentiate cancer cells tolerance to treatment (Hirata et al., 2015). Here, TNC is linked to cancer.