In UVB‐mediated immune response in keratinocytes, UVB exposure may increase TSLP expression through a HIF‐1α‐dependent mechanism.31 It has been reported that epithelial barrier dysfunction can lead to loss of adhesion between cells and cause the release of allergy‐related cytokines, such as TSLP, in skin keratinocytes.58 Recent research by our group showed that CLDN1 down‐regulation in HaCaT cells could exacerbate the production of TSLP.59 Calycosin may reduce the production of TSLP and IL‐33 by repairing the tight junctions. The gene discussed is IL33; the disease is allergic disease.