We focused on genes mediating selumetinib sensitivity as potentially druggable dependencies, and the top 2 conserved sensitivity hits were BRAF, a direct effector of Ras with established roles in glioma (16, 17, 37), and SHOC2, which has not been previously implicated in glioblastoma to our knowledge (Figure 4C). The gene discussed is BRAF; the disease is glioblastoma.