The recent discovery of paradoxical activation of the MAPK-pathway with RAF inhibitors in BRAF-wild type tumors [33] raises the possibility that the use of a RAF inhibitor (sorafenib) could even have been counter-productive in uveal melanoma with GNAQ/GNA11 mutations, and may have negated the potential therapeutic benefits of sorafenib through mechanisms other than MAPK-inhibition. Here, GNA11 is linked to uveal melanoma.