Rapid EGFR-mediated reactivation of the MAPK pathway has been connected to the relative insensitivity of BRAF-mutant colorectal carcinoma cells (CRCs) to vemurafenib, suggesting that combined BRAF and EGFR inhibition could be a promising therapeutic strategy to overcome one of the mechanisms of resistance to BRAF targeted therapies.41 Indeed, we show that co-treatment with an inhibitor of EGFR (as the last effector in the COX-PGE2-EGFR crosstalk) re-sensitises BRAF-mutant melanoma cells with acquired resistance to vemurafenib. The gene discussed is EGFR; the disease is melanoma.