In contrast to SLE, genetic predisposition to RA and PsA has not been linked to a polymorphism of IKZF1. Instead, accessibility at the IKZF1 promoter as well as several gene regulatory regions was reduced, independent of any disease-associated SNPs, supporting the notion that the reduced transcription of IKZF1 in naive CD4+ T cells is epigenetically determined and acquired. This evidence concerns the gene CD4 and rheumatoid arthritis.