TLR4 activation by different bacterial LPS induces production of inflammatory mediators in hPDLCs.22 Similarly, TLR2 activation results in cytokine production by PDLCs32 and gingival fibroblasts.33 Our finding is a further indication that hPDLCs cannot develop any immune tolerance state and this is additional evidence of their role in sustained inflammation in periodontal disease. The gene discussed is TLR4; the disease is periodontal disorder.