However, the combination of KRASG12C inhibition with anti-PD1 was only synergistic in the immunogenic tumor model (KPARG12C), but not in the two models that were intrinsically resistant to ICB, one “cold” tumor model lacking neoantigens (KPB6G12C) and one “T cell excluded” model that evades antitumor immunity by down-regulating MHC and recruiting immunosuppressive myeloid cells (3LL ΔNRAS). The gene discussed is PDCD1; the disease is neoplasm.