JUN and neoplasm: In this context, IL‐36γ also activates and IL‐36Ra antagonizes the MAPK signaling pathways (such as Jun) that synergize with NF‐κB for the induction of proinflammatory cytokines.[42, 43] Second, IL‐36γ and IL‐36Ra do not reciprocally regulate the expression of proinflammatory cytokines in the in vivo tumor models as they do in the in vitro cultures.