Studies in rodent models of sterile corneal inflammation upon injury have identified keratocyte-derived HSPB4 as an important DAMP that binds TLR2 on resident macrophages, initiating nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling to produce interleukins (ILs) and tumor necrosis factor-alpha (TNFα) [3]. This evidence concerns the gene CRYAA and inflammatory response.