BRAF and melanoma: In the present work we show that ErbB3 is central to a feedback survival loop activated in melanoma cells upon exposure to BRAF and/or MEK inhibitors, that this activation is dependent upon increased production and release of neuregulin by melanoma cells and, most importantly, that antibodies against ErbB3 capable to induce receptor degradation, abolish this loop and strongly potentiate the antitumor efficacy of BRAF and or MEK inhibitors when given in combination.