It has been reported that calycosin reduced NF‐κB activation in LPS‐stimulated human keratinocytes 44 and LPS induced HIF‐1α protein accumulation by activating NF‐κB.45 Moreover, the role of HIF‐1α in allergic diseases has been increasingly recognized.46, 47 A previous study showed that HIF‐1α increases epithelial permeability in human nasal epithelium.48 Moreover, tight junction proteins are indicated as MMP (matrix metalloproteinases) substrates. This evidence concerns the gene HIF1A and allergic disease.