The rationales for this combination were, firstly, that selumetinib has demonstrated preclinical efficacy in both BRAF wild-type and mutant melanoma models.14 Secondly, resistance to taxane-induced apoptosis can be mediated by MAPK pathway activation, and thus concurrent MEK1/2 inhibition may potentiate the efficacy of taxane chemotherapy. Here, BRAF is linked to melanoma.