The suggested therapeutic benefit from our data depicting diminished combined MEK/BRAF inhibitor resistance in MEK1 Q56P A375 cells, but not in the KRAS G13D or NRAS Q61K melanoma models is consistent with clinical data demonstrating the effectiveness of combined MEK/BRAF inhibitor therapy for the treatment of melanomas with secondary activating RAS mutations and acquired BRAF inhibitor resistance [5]. This evidence concerns the gene KRAS and melanoma.