The Kirsten RAt Sarcoma viral oncogene homologue(KRAS) is associatedwith a high mortality rate, for example, in pancreatic ductal adenocarcinoma(PDAC), non-small cell lung cancer (NSCLC), and colorectal cancer(CRC).1 Functionally, KRAS cycles betweenan inactive, GDP-loaded (KRAS “off”) and an active,GTP-loaded (KRAS “on”) state, with the latter mediatingdownstream effector signaling.2,3. The gene discussed is KRAS; the disease is colorectal cancer.