classification, and a suitable therapy would be given to patients by diagnosing with damps. the regulation of damp signaling can be a potential therapeutic target to reduce inflammation and treat diseases. for example, administration of neutralizing hmgb1 antibodies or truncated hmgb1-derived a-box protein ameliorated arthritis in collagen-induced arthritis rodent models. clinical trials with hsp inhibitors have also been reported. for nonsmall-cell lung cancer, hsp27, hsp70, and hsp90 inhibitors are under investigation in clinical trials. in addition, treatment with dnajp1, which is a synthetic peptide derived from dnaj (hsp40), had a curative effect in rheumatoid arthritis patients without critical side effects. taken together, damps can be useful therapeutic targets for various human diseases, including cancer and autoimmune diseases. damps can trigger re-epithelialization upon kidney injury', contributing to epithelial–mesenchymal transition, and potentially, to myofibroblast differentiation and proliferation. these discoveries suggest that damps drive not only immune injury, but also kidney regeneration and renal scarring. for example, tlr2-agonistic damps activate renal progenitor cells to regenerate epithelial defects in injured tubules. tlr4-agonistic damps also induce renal dendritic cells to release il-22, which also accelerates tubule re-epithelialization in aki. finally, damps also promote renal fibrosis by inducing nlrp3, which also promotes tgf-β receptor signaling.