This advantage has been exemplified in BRAF(V600)-mutant melanoma, colon, and thyroid carcinoma, whereby the formation of eIF4F translation initiation complexes was the common point of convergence of multiple pathways that conferred resistance to targeted anti-BRAF, anti-MEK, and anti-BRAF plus anti-MEK drug combinations (4). The gene discussed is BRAF; the disease is melanoma.