These studies suggest that specific inhibitors targeting KRAS (G12C) in tumour cells profitably result in a turn from an immunosuppressive to an immunocompetent TME; thus, the combination of KRAS (G12C) inhibitors and immune checkpoint inhibitors is a promising reciprocal strategy for patients with KRAS (G12C) mutant NSCLC. The gene discussed is KRAS; the disease is neoplasm.