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Lters binding affinity at the promoter, one at rs2004640 which creates an alternate splice site (exon 1B) in the untranslated first exon, another is a 30-bp in-frame insertion/deletion in exon 6, and the third is a 3'UTR polymorphism which creates an alternate polyadenylation site resulting in shorter and more stable mRNA. It has been demonstrated that these four variants combine to form a SLE ris

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