The choice of those melanoma cell lines was based on previous studies where adaptive upregulation of ErbB3 and PDGFR-β was observed following BRAF targeting, and those RTKs were associated with resistance to targeted therapy.16,20 Importantly, we show that an intermittent dosing schedule of PLX51107 was tolerable and prolonged the growth inhibition achieved by continuous BRAFi/MEKi treatment. Here, ERBB3 is linked to melanoma.