They include: (i) injury of KCs by the UV and gamma radiation1 that activates TFs NF‐κB and AP138; (ii) auto‐inflammatory skin diseases, such as the uncontrolled production of IL‐1β in the constitutive disorder of the skin and bones,28 (iii) an excessive expression of TSLP in the Netherton Syndrome,27 and (iv) early severe allergic disease resulting from the inborn errors of immunity due defective TFs.39 This evidence concerns the gene IL1B and allergic disease.