Despite the confirmed activation of the mitogen-activated extracellular-signal-regulated kinase (MEK/ERK) pathway in some of these tumors, it is not clear whether mutations in these putative BRAF-driven tumors confer upfront sensitivity to inhibitors of BRAF (BRAFi) and/or MEK (MEKi) or alter the tumor genetic composition21–23. This evidence concerns the gene MAP2K7 and neoplasm.