Overall our data lead to a model, whereby in tumours on treatment with BRAF inhibitor‐induced MITF up‐expression in MITF‐high cells increases intra‐tumour EDN1 levels, which can act on MITF‐high (paracrine or autocrine) as well as AXL‐high cells to re‐activate ERK (Fig 8L). This evidence concerns the gene BRAF and neoplasm.