KRAS

KRAS encodes KRAS proto-oncogene, GTPase (189 aa). Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Highest expression in Nerve Tibial (30.7 TPM) and Brain Cerebellar Hemisphere (25.1 TPM).

Autoimmune lymphoproliferative syndrome type 4 is associated with mutations in the KRAS gene on chromosome 12.

KRAS is classified as a druggable target (Clinically Actionable, Drug Resistance, and Enzyme categories) with score 1.0.

NRAS

NRAS encodes NRAS proto-oncogene, GTPase (189 aa). Ras proteins bind GDP/GTP and possess intrinsic GTPase activity Highest expression in Cells EBV-transformed lymphocytes (77.3 TPM) and Cells Cultured fibroblasts (52.5 TPM).

Autoimmune lymphoproliferative syndrome type 4 is associated with mutations in the NRAS gene on chromosome 1.

The NRAS protein participates in S-Farn-Me KRAS4A, HRAS, NRAS and S-Farn-Me PalmS KRAS4A,HRAS, NRAS pathways.

NRAS is classified as a druggable target (Clinically Actionable, Drug Resistance, and Enzyme categories) with score 0.8.

Genetic testing for KRAS, NRAS is available. Testing is considered confirmatory for diagnosis.

Biomarker and diagnostic research for autoimmune lymphoproliferative syndrome type 4 has been reported in the published literature.

Estimated prevalence: <1 in 1,000,000 (VERY_RARE).

1 clinical trial registered, 1 recruiting. Interventions under study include biologic therapy. Research is primarily sponsored by academic and government institutions.

33 publications have been identified in PubMed for autoimmune lymphoproliferative syndrome type 4. Research spans Basic Science / Preclinical (28%), Epidemiology / Natural History (28%), and Diagnostic / Biomarker (17%).

Recent Publications

• Okuda Y (2026). [PMID: 40971131](https://pubmed.ncbi.nlm.nih.gov/40971131/). *Clin Exp Nephrol*. [Epidemiology / Natural History]

• Bognár D (2026). [PMID: 42124462](https://pubmed.ncbi.nlm.nih.gov/42124462/). *J Magn Reson Imaging*. [Basic Science / Preclinical]

• Xu S (2026). [PMID: 41501749](https://pubmed.ncbi.nlm.nih.gov/41501749/). *BMC Endocr Disord*. [Basic Science / Preclinical]

• Schmitz EG (2026). [PMID: 41654260](https://pubmed.ncbi.nlm.nih.gov/41654260/). *J Allergy Clin Immunol*. [Basic Science / Preclinical]

• Ariue B (2026). [PMID: 41057108](https://pubmed.ncbi.nlm.nih.gov/41057108/). *Ann Allergy Asthma Immunol*. [Diagnostic / Biomarker]

• Veith PD (2026). [PMID: 41992463](https://pubmed.ncbi.nlm.nih.gov/41992463/). *Microbiologyopen*. [Basic Science / Preclinical]

• Mülküt F (2025). [PMID: 40002606](https://pubmed.ncbi.nlm.nih.gov/40002606/). *Diagnostics (Basel)*. [Diagnostic / Biomarker]

• Knapp J (2025). [PMID: 40161289](https://pubmed.ncbi.nlm.nih.gov/40161289/). *Resusc Plus*. [Epidemiology / Natural History]

• Gallhammer F (2025). [PMID: 40605520](https://pubmed.ncbi.nlm.nih.gov/40605520/). *Parasitology*. [Epidemiology / Natural History]

• Fernandes S (2025). [PMID: 40604745](https://pubmed.ncbi.nlm.nih.gov/40604745/). *BMC Public Health*. [Epidemiology / Natural History]