Similar to the proinflammatory responses observed in this colon cancer model (6, 7), our previous work also revealed remodeling of the TME following KRAS-G12C inhibition in multiple lung tumor models, including the immune cold orthotopic Lewis lung murine NSCLC tumor model that was genetically engineered to disrupt the NRAS gene, avoiding redundancy in RAS signaling (3LL ΔNRAS, here referred to as 3LL in short) (8, 9). The gene discussed is KRAS; the disease is malignant colon neoplasm.