Systemic lupus erythematosus (SLE) is an autoimmune disorder with multifactorial etiology characterized by a high level of antibodies directed against nuclear and other cellular antigens, multisystem inflammation, relapsing, and a variable course and prognosis. 1,2 Over 90% of cases of SLE occur in women, frequently starting during reproductive age (range 20-30 years). However, the peak of disease incidence among males is more than the age of 45 years. 3 Most common SLE manifestations include renal involvement, arthritis, serositis, hematological, neurological, skin lesions, and oral ulcers. 1,4 Several pieces of research show that genetic factors have an important part in the incidence of SLE. Twin studies report a concordance rate ranging 24%-35% for monozygotic twins and 2%-5% for dizygotic twins. 5 On the other hand, there is the familial aggregation of SLE, which means people with lupus often have family members with SLE or other autoimmune conditions (10%-20% compared to 1% of controls). 6,7 Recently, genome-wide association studies (GWAS) reported multiple single nucleotide polymorphisms and novel rare variants in several genes which have an immunological function in correlation with SLE risk. For example, 1 study reported rare variations in 98 SLE-associated
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