What you carry at this position in your DNA and what research says about it.
Somatic Cancer Gene: 3/10 evidence, 0 publications.
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Sample genotype (not yours): C/C
Typical Inherited KRAS Sequence
Your inherited copies of KRAS do not carry the codon 13 change. KRAS changes that matter in cancer are almost always SOMATIC - acquired by a tumour during life, not inherited - so this result says nothing about the KRAS status of any tumour, and nothing about how a tumour would respond to anti-EGFR therapy. That is established by testing tumour tissue.
What this genotype means: Normal KRAS protein function; Typical response to anti-EGFR therapies; No elevated risk of RASopathies.
Sample genotype (not yours): C/G
Inherited KRAS Codon 13 Change Reported
A codon 13 change is reported on one inherited copy of KRAS. This is unusual: codon 13 changes are overwhelmingly somatic, arising in tumour tissue. Inherited changes in KRAS are instead associated with the RASopathy developmental syndromes. A finding like this warrants clinical-grade confirmation, and it does not describe any tumour's KRAS status.
What this genotype means: Constitutively active KRAS signaling; Resistance to anti-EGFR cancer therapies; Increased risk of RASopathies if germline.
Sample genotype (not yours): G/G
A codon 13 change is reported on both inherited copies of KRAS. This is exceptionally unusual and, on array data, is more likely a genotyping artifact than a real inherited finding - codon 13 changes are overwhelmingly somatic. It warrants clinical-grade confirmation, and it does not describe any tumour's KRAS status.
What this genotype means: Constitutively active KRAS signaling; Resistance to anti-EGFR cancer therapies; Severe developmental risks if germline.
Gene function and biological role
Gene Function: The KRAS gene encodes a GTPase protein that plays a critical role in the RAS-MAPK signaling pathway, regulating cell growth, division, and survival. It acts as a molecular switch, cycling between an active GTP-bound state and an inactive GDP-bound state. Germline mutations in this gene can cause developmental disorders known as RASopathies, including Noonan syndrome and cardiofaciocutaneous syndrome. Somatic mutations are highly prevalent in various cancers, particularly colorectal, pancreatic, and lung cancers.
Variant Impact: The rs112445441 variant represents a nucleotide change at codon 13 of the KRAS gene, resulting in an amino acid substitution from glycine to alanine. This substitution alters the catalytic G-domain of the KRAS protein, impairing its ability to hydrolyze GTP and keeping the protein constitutively active. This continuous signaling drives uncontrolled cell proliferation and survival. In clinical oncology, codon 13 mutations are critical biomarkers used to predict resistance to anti-EGFR therapies.
Key Insight: Codon 13 mutations in KRAS act like a broken molecular switch, keeping cell growth signals permanently turned on.
Location: KRAS. Chromosome 12 · 12p12.1 · 25.2 Mb
Estimated prevalence by population
No frequency data available
This variant is not present in the gnomAD database.
Showing effects for C/C genotype
Rare Genetic Disorders
Congenital Malformations
RASopathy Risk. Evidence: 3/10. Typical Risk.
Showing effects for C/G genotype
RASopathy Risk. Evidence: 3/10. Elevated Risk.
Showing effects for G/G genotype
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Two copies of the normal, wild-type KRAS gene are present at codon 13 in this profile. This is the most common genetic status in the general population and represents the healthy baseline. Lacking the activating G13A mutation means there is no elevated risk of RASopathies like Noonan syndrome or cardiofaciocutaneous syndrome associated with this variant. Furthermore, in the event of a colorectal cancer diagnosis, tumors that are wild-type for KRAS are typically sensitive to anti-EGFR monoclonal antibody therapies such as cetuximab and panitumumab. This status is considered the neutral, healthy baseline.
Normal KRAS protein function; Typical response to anti-EGFR therapies; No elevated risk of RASopathies.
Sample genotype: CG (Heterozygous)
One copy of the activating G13A mutation in the KRAS gene is present in this profile. In a germline state, this mutation is extremely rare and can lead to developmental disorders known as RASopathies, such as Noonan syndrome or cardiofaciocutaneous syndrome. In oncology, this mutation is more commonly found as a somatic (acquired) mutation within tumor tissue, particularly in colorectal and lung cancers. The presence of this mutation keeps the KRAS protein in a permanently active state, driving tumor growth and rendering the cancer resistant to anti-EGFR therapies like cetuximab.
Constitutively active KRAS signaling; Resistance to anti-EGFR cancer therapies; Increased risk of RASopathies if germline.
Sample genotype: GG (Homozygous)
Two copies of the activating G13A mutation in the KRAS gene are present in this profile. This genetic status is exceptionally rare in the general population and may be embryonic lethal or associated with severe developmental disorders if present in the germline. In tumor tissue, homozygous KRAS mutations can occur during cancer progression, leading to highly aggressive tumor growth and complete resistance to anti-EGFR therapies like cetuximab and panitumumab. The mutation prevents the KRAS protein from turning off, resulting in continuous downstream signaling for cell proliferation. Oncologists use tumor genetic testing to identify such mutations and avoid ineffective treatments.
Constitutively active KRAS signaling; Resistance to anti-EGFR cancer therapies; Severe developmental risks if germline.
Variants with shared genetic architecture
rs121913529 · KRAS Gene · Chr 12 · Cancer Risk
rs121913530 · KRAS Gene · Chr 12 · Lung Cancer Risk
rs5011804 · KRAS Gene · Chr 12 · Brain Volume and Health
Content updated August 2026.
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