Thus, vemurafenib-resistant cells characterised by mitogen-activated protein kinase (MAPK) reactivation through expression of aberrantly spliced mutated BRAF protein exhibiting kinase activity.18 Also, other mechanisms of melanoma BRAF resistance underlie BRAF amplification.19 and the activation of the prooncogenic signalling pathway.20 The gene discussed is BRAF; the disease is melanoma.