Considering a recent report that the loss of RAGE contributes to pulmonary fibrosis [31], the increase of HMGB1 in alveolar fluids itself may induce fibrogenesis through other HMGB1 receptors, such as the Toll-like family of receptors (TLRs), TLR4, TLR2, or TLR9 [32, 33]. The gene discussed is TLR2; the disease is pulmonary fibrosis.