Together, these data suggest that AMG510 and anti-PD-1 combination therapy can establish an adaptive immune response against shared antigens that can recognize and eliminate related but non-KRASG12C tumors as well, a clinically relevant outcome since intratumoral KRAS mutation status can be heterogeneous within the same tumor and between primary and metastatic sites [95–100]. The gene discussed is PDCD1; the disease is neoplasm.