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KRAS gene
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Gene

KRAS gene

The KRAS gene provides instructions for making the K-Ras protein, a GTPase that acts as an on/off switch for cell growth and division signaling pathways.

Normal Function

The KRAS gene provides instructions for making a protein called K-Ras that is part of the RAS/MAPK signaling pathway. This protein relays signals from outside the cell to the nucleus, instructing the cell to grow, divide, or mature. K-Ras acts as a switch: it is turned on when bound to a molecule called GTP and turned off when it converts GTP to GDP. When bound to GDP, it does not relay signals to the nucleus.

The KRAS gene is an oncogene. When mutated, it has the potential to cause normal cells to become cancerous. It plays important roles in cell division, differentiation, and apoptosis (self-destruction of cells).

Health Conditions Related to Genetic Changes

Cardiofaciocutaneous syndrome

Mutations in the KRAS gene are an uncommon cause of cardiofaciocutaneous syndrome. These germline mutations are present in all body cells and change single amino acids in the K-Ras protein. The altered protein shows increased GTP binding and a decreased ability to convert GTP to GDP, leading to prolonged activation of the protein and altered signaling that interferes with organ and tissue development.

Lung cancer

At least three somatic mutations (acquired during a lifetime and present only in tumor cells) in the KRAS gene are associated with lung cancer. These mutations result in a K-Ras protein that is constantly turned on (constitutively activated), directing cells to proliferate uncontrollably. These mutations are found in 15 to 25 percent of all lung cancer cases and are more common in long-term tobacco smokers. Lung cancers with these mutations typically indicate a poor prognosis and resistance to several cancer treatments.

Other cancers

Somatic mutations in the KRAS gene are involved in the development of several types of cancer, particularly pancreatic and colorectal cancers. These mutations lead to a K-Ras protein that is more strongly overactivated than the mutations that cause cardiofaciocutaneous syndrome, resulting in uncontrolled cell proliferation.

Other disorders

Germline mutations in the KRAS gene can cause a KRAS mutation-associated phenotype, which overlaps with cardiofaciocutaneous, Noonan, and Costello syndromes. Features include mild to moderate intellectual disability, distinctive facial features, short stature, macrocephaly, and sparse, thin hair. These mutations abnormally activate the protein, interfering with normal development.

Other Names for This Gene

  • C-K-RAS
  • c-K-ras protein
  • c-K-ras2 protein
  • c-Kirsten-ras protein
  • cellular c-Ki-ras2 proto-oncogene
  • K-ras p21 protein
  • KI-RAS
  • Kirsten rat sarcoma viral oncogene homolog
  • KRAS1
  • PR310 c-K-ras oncogene
  • RASK2
  • RASK_HUMAN
  • transforming protein p21
  • v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog

Frequently Asked Questions

Patients with KRAS‑mutated lung cancers often present as long‑term smokers or former smokers, and the tumors tend to be adenocarcinomas located in the peripheral lung fields. Imaging may show a solid or part‑solid nodule, but the definitive clue is a history of heavy tobacco use combined with a non‑small cell lung cancer diagnosis. Genetic testing of the tumor tissue is required to confirm the mutation.
KRAS itself is difficult to target directly, so most therapies focus on downstream pathways such as MEK or ERK inhibitors. However, KRAS mutations are associated with resistance to EGFR‑tyrosine kinase inhibitors, so patients with KRAS‑positive tumors are usually not offered EGFR‑TKIs. Clinical trials are exploring KRAS G12C inhibitors (e.g., sotorasib, adagrasib) that specifically bind the mutant protein.
The primary risk factor for KRAS mutations in lung cancer is smoking. Quitting smoking dramatically reduces the chance of developing KRAS‑driven tumors. Other factors such as occupational exposures to carcinogens or radon may also contribute, so minimizing exposure to these risks can help. A healthy diet, regular exercise, and avoiding environmental pollutants further support overall lung health.
KRAS mutations are generally associated with a poorer overall survival compared with KRAS‑wild‑type tumors, partly because they are less responsive to conventional chemotherapy and targeted agents. Patients with KRAS mutations should be monitored closely for disease progression and may be eligible for clinical trials of novel KRAS inhibitors or combination therapies. Regular imaging and tumor marker assessments are recommended as part of routine follow‑up.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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