KRAS and neoplasm: While “driver” mutations in oncogenes and tumor suppressors, such as IDH1, KRAS and TP53, can give rise to antigenic neo-epitopes [4–6], “passenger” mutations resulting from dysregulated tumor DNA replication/repair processes, and that are elevated in environmentally exposed tissue sites (e.g. skin, lung, colon), are thought to provide the greatest source of neo-epitopes [7].