Furthermore, both in melanoma tissues and cell lines, the BRAF inhibitor was found to be more potent as a PTK inhibitor than as a STK inhibitor, in accordance with Tahiri et al, who found higher inhibition of PTK activity by vemurafenib in V600EBRAF melanoma than in BRAF WT [42], indicating that V600EBRAF mainly activates signalling pathways implicating tyrosine kinases. The gene discussed is BRAF; the disease is melanoma.