Skin wounds from ischemia-reperfusion injuries — tissue damage caused by blood returning to tissues after a period of oxygen deprivation — may not heal appropriately in some patients, owing to elusive underlying immunological mechanisms. Scientists from Japan have now succeeded in proposing a means to solve this medical conundrum by understanding the role of interleukin-36 receptor antagonists as they act to inhibit the effects of interleukin-36 cytokines, which could help identify new therapeutic targets for wound healing.