These data corroborate similar findings demonstrating increased responsiveness of MITFHigh melanoma cells to MAPK signaling inhibitors.22 Although these results may argue for MAPK inhibition as a sufficient means to overcome MITF-associated features, in light of a recent report demonstrating BRAF-i-mediated MITF induction,17 and the highly pervasive acquired resistance to targeted BRAF inhibition,5, 6, 7, 8, 9 identification of new targets able to simultaneously overcome/bypass MITF and BRAF(V600E) activities is essential. The gene discussed is MITF; the disease is melanoma.