A recent breakthrough came with the BRAF inhibitor vemurafenib, which achieved high response rates in BRAF‐mutated metastatic melanoma.2 Interestingly, BRAF inhibition in RAS‐mutated tumors induces paradoxical ERK activation and tumor progression owing to the formation of RAF dimers.3 RAF dimerization is also a major mechanism of acquired clinical resistance to RAF inhibitors.4 Owing to its important clinical implications, RAF dimerization has attracted enormous interest. Here, RAF1 is linked to neoplasm.