Crohn's disease (CD) is a subtype of inflammatory bowel disease (IBD) characterized by chronic inflammation of the intestinal lining. It is believed to result from an abnormal immune system response to bacterial flora in the intestines of genetically predisposed individuals. Clinically, CD patients may experience abdominal pain, diarrhea, fever, weight loss, bloody stools, and pain with bowel movements. A diagnosis of CD is typically based on a clinical evaluation, as well as laboratory data, radiographic studies, endoscopic imaging, and histopathology. However, it is often difficult to distinguish CD from ulcerative colitis (UC), another form of IBD. As a result, approximately 10% of patients are initially classified as having indeterminate colitis. Multiple genes and environmental factors are believed to play a role in CD susceptibility. The first gene found to be associated with CD is the gene encoding the nucleotide-binding oligomerization domain protein 2, NOD2 (also known as CARD15, or caspase recruitment domain-containing protein 15), which is located on chromosome 16 at band q12. The NOD2 protein functions in the recognition of bacterial peptidoglycans, which leads to an immune response through activation of the nuclear factor-B (NFB) transcription factor. Three variants in the NOD2 gene are known to be associated with an increased risk for CD: p.Arg702Trp (c.2104C>T), p.Gly908Arg (c.2722G>C), and p.Leu1007fs (c.3020insC). Although the precise mechanism is not clearly understood, these NOD2 variants are thought to result in an exaggerated immune response and, eventually, chronic inflammation of the intestinal mucosa. There is no cure for CD and currently no way to prevent the onset of the disease. Treatment, which may include surgery and anti-inflammatory medications, is typically lifelong but may result in periods of remission.