The results indicate that human melanoma cells rendered resistant to the BRAFi vemurafenib express higher levels of VEGFR‐1 compared to their BRAFi‐sensitive counterparts and that inhibition of VEGFR‐1 with D16F7 mAb might be a suitable adjunct therapy for VEGFR‐1 positive tumours with acquired resistance to vemurafenib. This evidence concerns the gene FLT1 and melanoma.