Macrophage-derived meteorin-like promotes skeletal muscle repair. Macrophages are professional phagocytes that secure host defense. In parallel, these innate immune cells aid healing responses. The crucial importance of macrophages during muscle repair has recently received a lot of attention. Yet, macrophage functions during healing are so diverse that it has remained difficult to delineate precise mechanisms. Indeed, macrophages play crucial roles at both the initial inflammatory phase of muscle repair to clear injury-related debris and during the subsequent regenerative phase by promoting myofiber expansion. Unraveling the factors that coordinate this macrophage phenotype switching could not only reveal new targets to promote muscle repair but could also provide new ways to therapeutically reshape deranged macrophage activation in other settings. In a recent study, Bath et al. describe meteorin-like (METRNL) as an important regulator of skeletal muscle regeneration. METRNL is a protein that was originally shown to be produced in response to physiological stimuli to stimulate thermogenesis. Now, the authors show that METRNL is induced in damaged human muscle after resistance training and use whole-body and cell-specific Metrnl knock-out mice to further delineate the role of METRNL during muscle repair. In performing parabiosis experiments, bone marrow transplantations, and single-cell RNA sequencing, as well as using recombinant METRNL, the authors surprisingly found that mainly macrophage-derived METRNL mediated muscle repair in mice. Within macrophages, METRNL induced a proresolving phenotype and elicited insulin-like growth factor 1 production. This growth factor increased muscle stem cell proliferation and, as such, macrophage-mediated METRNL induction was shown to facilitate successful muscle regeneration. The potential translational relevance of this study lies in the observation that METRNL is induced in injured human muscle; the main caveat of this study is that the findings obtained in genetic models still need to be validated in humans. Another outstanding question is which stimuli trigger Metrnl expression in macrophages, and whether also other inflammatory insults can induce Metrnl. Last, these new findings raise the question whether METRNL could be employed to reprogram pro-inflammatory into anti-inflammatory macrophages and, as such, serve as a new therapeutic target for inflammatory diseases not directly related to muscle repair.