These findings suggest that bacteria have several key pathogenic roles in rosacea: they (a) activate TLR2 on KCs to upregulate KLK5 (10), (b) provide an essential source for nucleic acid in order to activate pDCs to produce type I IFN and initiate a pathogenic inflammation, and (c) activate neutrophils through cell-surface TLRs (8). The gene discussed is KLK5; the disease is rosacea.