Taken together, genome-wide CRISPRi screens suggest cell cycle dysregulation is essential for NF1-mutant glioblastoma growth and compensatory Ras activation underlies MEK inhibitor responses, with SHOC2 constituting a potential additional therapeutic target to maximally block Ras pathway output and enhance selumetinib responses in glioblastoma. The gene discussed is MAP2K7; the disease is glioblastoma.