**7. Conclusion**

Chronic inflammatory bowel disease is a subject of great interest among researchers because the pathomechanism of these conditions is difficult to explain, and thus far there is no optimal therapeutic process completely eliminating the symptoms and effects of the disease [37, 38].

Epidemiological and clinical studies suggest that the pathogenesis of inflammatory bowel disease is strongly linked to genetic predisposition [39, 40].

CD and UC are considered polygenic diseases in which familial clustering is observed in 5–10% of patients [41].

Among genetic factors associated with IBD development, it has been found that many single-nucleotide polymorphisms are associated with susceptibility to IBD progression. SNP can affect the production or function of a protein and thus affect the development of the disease [14].

However, although the overall role of genes involved in the development of IBD is already in most cases known, as of today it is unclear how the SNPs in these genes affect cellular function, or how such changed cellular functions would contribute to the development of IBD [27]. Therefore, further research is needed to demonstrate how gene polymorphism leads to the development of IBD.
