BRAF and cancer: Prete and others (Prete et al., 2018) demonstrated that in cancer cells with BRAF mutations, therapeutic escape from BRAFi/MEKi was facilitated by pericytes that secreted thrombospondin-1 (TSP-1) and TGF-β1, both of which led to a rebound of pERK1/2, pAKT and pSMAD3 (Fedorenko et al., 2015).