The clinical use of BRAF inhibitors (vemurafenib, dabrafenib, encorafenib), MEK inhibitors (trametinib, cobimetinib, binimetinib) or their combinations significantly increase progression-free and overall survival of patients.3,4 Unfortunately, most patients develop resistance to these inhibitors soon after the start of therapy5,6 because of different factors including tumour heterogeneity and plasticity.7 The gene discussed is BRAF; the disease is neoplasm.