Rheumatoid arthritis (RA) is a systemic, inflammatory, and chronic disease characterized by a persistent immune response that leads to inflammation and destruction of joints. The etiopathogenic mechanisms involved are complex and include an interaction between the innate and acquired immune response, involving antigen-presenting cells (APCs), autoreactive T cell formation, and production of autoantibodies directed against their own cellular structures, like rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPAs). These antibodies are often present in the blood, long before any sign of joints’ inflammation, suggesting that the triggering of autoimmunity might occur at different sites to the joints, for example, the gastrointestinal tract or airway [1]. Epidemiological studies suggest rheumatoid arthritis as the result of complex interactions between genes, environmental and hormonal factors, and the immune system [2, 3]. There is a genetic susceptibility to rheumatoid arthritis by a tendency to familial aggregation, a concordance between monozygotic twins and an association with some histocompatibility antigens [4, 5]. Heritability estimates have suggested a 60–۷۰% genetic risk factors, responsible for developing rheumatoid arthritis [6]. Candidate gene or genome-wide association studies have identified different risk loci associated with rheumatoid arthritis etiology. Currently, in this disease, about 100 described genes are associated with susceptibility, protection, severity, activity, and treatment response [6]. Human leukocyte antigen (HLA) polymorphisms are the most important genetic risk factors. HLA are an important part of the immune system triggering T cells of the immune system to produce antibodies. Associations of RA with HLA-DRB1 alleles have been observed in all racial and ethnic populations [7, 8].