**7. Conclusion**

From a genetic perspective, several molecules involved in the response to pathogens and multiple genes that activate or regulate inflammation appear to be critical in the etiopathogenesis of BD. However, the precise pathogenic mechanisms of these genes on BD are still unclear. In addition, it is unknown how genetic components as well as other associated risk factors such as bacterial and viral pathogens affect the developmental process of BD. Genome-wide association studies (GWAS) have become a very important step in understanding BD pathogenesis. GWASs with satisfactory numbers of subjects in regions where BD is prevalent revealed a strong association between BD and inflammatory cytokines such as IL-1, IL-4, IL-6, IL-10, IL-17, and IL-23–IL-12RB2. Some association studies, for example TNFAIP3, TLRs and miRNAs, appear to be conflict in different study groups and/or populations. The conflicting results of these genes associated with BD suggest that they may be ethnically specific or have occurred due to sample selection bias. In the future, similar studies in different populations with a higher number of patients will provide significant advances in the etiopathology of BD. We proposed that genetic factors located at loci outside the MHC region (IL1A-IL1R, IL10, CCR1-CCR3, ERAP1, IRF8, RIPK2, FUT2, IL-28, IL-29, NOD1, NOD2, VEGF and etc.…) contributed to BD susceptibility by playing a role in host defense and immune responses to pathogens in inflammation pathways. Moreover, specific gene polymorphisms have been linked with clinical presentation of BD such as ocular lesions, neurological and intestinal and cardiovascular involvement. The future direction will guide possible therapeutic approaches by understanding the functional significance of BD-associated gene polymorphisms, as well as insights into the pathogenesis of the disease.
