In majority of claimed cancer ‘targeted’ therapies, ‘personalized’ or ‘precision’ medicine or the recently fashionable immunotherapeutic approaches, drugs are developed as inhibitors of one or combination of specific over‐, or under‐expression of cancer-associated molecules such as various proteins, epitopes, growth factors, cytokines/chemokines, receptor/adaptor molecules or enzymes (e.g., Kras, BCR, PI3K, CD11, CD22, Myc, BRCA2, ALK, IL-10, IL-12, p53, p27, p70, MAPKs, TKIs, VEGF, EGF), identified in the molecular tsunami of site-specific cancers [18–22, 27–39, 43–45, 65, 66]. This evidence concerns the gene KRAS and cancer.