Inflammation is a body's response to harmful stimuli that aims to eliminate the trigger that caused the initial injury and enable tissue repair. Inflammation can be either pathogen-associated or sterile. Sterile inflammation can be triggered by acute conditions, such as trauma, toxin exposure, and ischemia-reperfusion injury, but it is also an important component of life-threatening chronic inflammatory conditions, such as atherosclerosis, cancer, and asbestosis (1). Regardless of etiology, the mechanisms resolving inflammatory responses constitute highly coordinated and active processes that are vital for restoring tissue homeostasis. Although the cellular and molecular signals that drive the initiation of sterile inflammation are well studied (1), we have a relatively poor understanding of the mechanisms through which sterile inflammation is resolved, thus limiting our ability to therapeutically tackle harmful inflammation. On page 111 of this issue, Wang et al. (2) shed light on a provocative aspect of resolution by key orchestrators of the inflammatory process: neutrophils.