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===Genetic factors=== Genetic factors such as HLA-DR1B1,<ref>{{cite journal | vauthors = Raychaudhuri S | title = Recent advances in the genetics of rheumatoid arthritis | journal = Current Opinion in Rheumatology | volume = 22 | issue = 2 | pages = 109β118 | date = March 2010 | pmid = 20075733 | pmc = 3121048 | doi = 10.1097/bor.0b013e328336474d }}</ref> [[TRAF1]], PSORS1C1 and [[microRNA]] 146a<ref>{{cite journal | vauthors = Conigliaro P, Triggianese P, De Martino E, Fonti GL, Chimenti MS, Sunzini F, Viola A, Canofari C, Perricone R | title = Challenges in the treatment of Rheumatoid Arthritis | journal = Autoimmunity Reviews | volume = 18 | issue = 7 | pages = 706β713 | date = July 2019 | pmid = 31059844 | doi = 10.1016/j.autrev.2019.05.007 | hdl-access = free | s2cid = 146811143 | hdl = 2108/225718 }}</ref> are associated with difficult to treat rheumatoid arthritis, other gene polymorphisms seem to be correlated with response to biologic modifying anti-rheumatic drugs (bDMARDs). Next one is FOXO3A gene region been reported as associated with worst disorder. The minor allele at FOXO3A summon a differential response of monocytes in RA patients. FOXO3A can provide an increase of pro-inflammatory cytokines, including TNFΞ±. Possible gene polymorphism: STAT4, PTPN2, PSORS1C1 and TRAF3IP2 genes had been correlated with response to TNF inhibitors.<ref>{{cite journal |last1=Conigliaro |first1=Paola |last2=Ciccacci |first2=Cinzia |last3=Politi |first3=Cristina |last4=Triggianese |first4=Paola |last5=Rufini |first5=Sara |last6=Kroegler |first6=Barbara |last7=Perricone |first7=Carlo |last8=Latini |first8=Andrea |last9=Novelli |first9=Giuseppe |last10=Borgiani |first10=Paola |last11=Perricone |first11=Roberto |date=2017-01-20 |editor-last=Ahuja |editor-first=Sunil K |title=Polymorphisms in STAT4, PTPN2, PSORS1C1 and TRAF3IP2 Genes Are Associated with the Response to TNF Inhibitors in Patients with Rheumatoid Arthritis |journal=PLOS ONE |language=en |volume=12 |issue=1 |pages=e0169956 |doi=10.1371/journal.pone.0169956 |issn=1932-6203 |pmc=5249113 |pmid=28107378 |bibcode=2017PLoSO..1269956C |doi-access=free }}</ref>
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