The majority of strategies for treating KRAS-mutated cancers are based on indirect therapies targeting, for example, the nucleotide exchange, membrane receptors, metabolic rewiring, and other effectors (RAF, MEK, PI3K, mTOR, FAK, EGFR, etc.)of signaling pathways in which KRAS is involved such as MAPK or EGFR [20,21,22]. The gene discussed is KRAS; the disease is cancer.