Subsequent studies examining the effectiveness of PLX8394 in lung adenocarcinomas, where 40% of B-Raf mutant tumours have non-V600 mutations, found that this drug could inhibit signalling driven by V600 or non-V600 mutants, and could suppress the growth of vemurafenib-resistant lines expressing the dimeric V600E-B-Raf splice variant (Okimoto et al, 2016). This evidence concerns the gene BRAF and neoplasm.