FOS can increase the risk of recurrence of IBD66; one variant identified in the IBD cohort is located at the exon of ETV6; IRF1 and ETV6 are key TFs with activity differences in IBD67; genes FOS, FOSB and JUN encode potent mediators of IBD68; CUX1 is induced in IBD69; and STAT1 epigenetically contribute to the pathogenesis of IBD70. This evidence concerns the gene JUN and inflammatory bowel disease.