When bypassing BRAFV600E activity, resistant melanomas often exhibit reactivation of the interconnected MAPK and PI3K/Akt axes, associated with BRAF-independent reactivation of MAPK [7] (caused in some cases by enhanced CRAF [8]), elevated PDGFR [9], and remodeling of the cancer stroma [10]. This evidence concerns the gene BRAF and melanoma.