Finally, the reduced activity towards dimeric Raf together with the ability to promote Ras-dependent Raf dimerisation provides an explanation for why vemurafenib and dabrafenib have had limited activity in tumour types with upregulated RTK or Ras signalling even when these tumours possess V600-B-Raf mutations (Girotti and Marais, 2013). The gene discussed is BRAF; the disease is neoplasm.