Moreover, BRAF inhibitors drive RAS-dependent BRAF binding to CRAF, CRAF activation, and MEK-ERK signaling in oncogenic RAS [18] revealing a paradigm of BRAF-mediated signaling that promotes tumour progression with clinical implications [38] and highlighting the importance of understanding pathway signaling in clinical practice and of genotyping tumours prior to administering BRAF-selective drugs, to identify patients who are likely to respond and also to identify patients who may experience adverse effects such as increased invasion [33]. This evidence concerns the gene RAF1 and neoplasm.