In the study of IL‐1β‐induced inflammatory mediators and NF‐κB‐induced effects on human gingival fibroblasts (HGFs), Vardar‐Sengul et al. [50] found that the gene expression changes induced by IL‐1β were consistent with the pathological changes of periodontitis, including the increase of inflammatory factors, driving factors, transcription factors, matrix metalloproteinases and adhesion molecules, especially the increase of NF‐κB‐dependent antiapoptotic factors. The gene discussed is IL1B; the disease is periodontitis.