The current clinical BRAF inhibitors vemurafenib and dabrafenib bind all RAF isoforms in kinase assays, but only inhibit proliferation and ERK signalling in BRAF V600E mutant cells.25 However, vemurafenib and dabrafenib caused a paradoxical induction of p-ERK and induce proliferation in BRAF wild type cells.26, 27 Here, we demonstrated that AZ304, a novel BRAF/BRAF V600E inhibitor, had anti-proliferative effects on both BRAF mutant and wild type tumours in vitro and in vivo. Here, RAF1 is linked to neoplasm.