In this context, various stimuli that activate NF‐κB and AP‐1 have been implicated in upregulation of IL‐36γ, including pattern‐recognition receptors (PRRs)‐mediated signaling and pro‐inflammatory cytokines‐mediated signaling that can be generated by enhanced genome instability or cell death in accompany with tumor progression.[29, 49, 50] Alternatively, ROS are increased in tumor cells and have been shown to activate NF‐κB and AP‐1,[17] which might upregulate IL‐36γ for GSH biogenesis and adaptation to oxidative stress (discussed below). Here, JUN is linked to neoplasm.