MAPK3 and synovial sarcoma: However, a number of our findings suggest that it is unlikely that activation of ERK1/2 results from upstream signalling elements and activating mutations in acquired pazopanib-resistant SS cells: PDGFRα was not activated more in pazopanib-resistant SS cells than in parental SS cells (Fig. 4a), pazopanib was still able to inhibit the phosphorylation of PDGFRα in pazopanib-resistant SS cells (Fig. 4a), phosphorylation of ERK1/2 was partially inhibited by pazopanib (Fig. 4a), and there were no identified gatekeeper mutations of PDGFRα in both of the resistant clones (Supplementary Figure 1).