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. Here, MCL1 is linked to neoplasm.