To this end, there is strong preclinical data to support that targeting MAPK pathway using MEK inhibitors increased tumor neo-antigen expression, intratumoral effector T cell infiltration, and synergy with PD1 blockade in CRC models.[50,51] Nonetheless, combining cobimetinib, a MEK inhibitor, with atezolizumab, a PD-L1 inhibitor, did not produce meaningful clinical benefit in patients with chemorefractory CRC in a recent Phase III study.[12] However, combining MEK inhibitors with other immunomodulatory agents remains a potential therapeutic strategy to bolster immune response in this setting. The gene discussed is CD274; the disease is neoplasm.