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. The gene discussed is IL36RN; the disease is neoplasm.