Preclinically, KRAS inhibitors have been associated with promotion of a proinflammatory tumor microenvironment, increased major histocompatibility complex class I protein expression, and synergies with immunotherapy to enhance antitumor activity.44,45,46 Moreover, KRAS inhibition has played a role in decreased myeloid-derived suppressor cells and increased classically activated M1-polarized macrophages, dendritic cells, cluster of differentiation (CD) 4+ cells, and CD8+ T cells, which are associated with tumor sensitivity to immune checkpoint inhibition.45 The gene discussed is KRAS; the disease is neoplasm.