While triggering of an immune “hot-start” by ICD-inducing chemotherapeutics improves the immunogenicity of the landscape, the supply of endogenous tumor-associated antigens (TAAs) (e.g., carcinoembryonic antigen and mesothelin) or neoantigens (e.g., KRAS and p53) may not suffice to educate high-affinity cytotoxic T lymphocytes (CTL) recruited to the primary cancer site from regional lymphoid structures. Here, KRAS is linked to neoplasm.