Regarding gastrointestinal carcinogenesis, histone lysine demethylase 4B (KDM4B) physically interacts with c-Jun at the promoter loci of IL-8, MMP1, and ITGAV through its demethylation activity, and infection with Helicobacter pylori results in a significant increase in the occupancy of KDM4B and c-Jun, leading to a significant attenuation of H3K9me3 signaling (22). This evidence concerns the gene JUN and infection.