Excitingly, this phenomenon can be exploited in vivo, as treatment of xenograft models of BRAF mutant melanoma with the RAF inhibitor dabrafenib induced an MCL-1 dependency in surviving tumor cells that could be exploited through subsequent treatment with the MCL-1 inhibitor S63845 to eradicate these cells, leading to tumor growth inhibition and survival that substantially exceeded what could be achieved with either agent alone6. This evidence concerns the gene BRAF and melanoma.