One possible cause for the lack of efficacy of PLX8394 in some BRAF fusion cancers could be that BRAF:BRAF homodimers each contain the constitutively primed NtA region meaning that, even though one partner may be inhibited by PLX8394, transactivation of the dimer partner may still be possible if this interaction is stabilised by dimerisation of the 5′ fusion partner. This evidence concerns the gene BRAF and cancer.