A team from CNIC and Yale reported in Journal of Experimental Medicine that neutrophils follow a circadian program that alters their aggressiveness, making nighttime neutrophils less damaging after myocardial infarction. The researchers showed that ATI2341, a pharmacological agonist targeting a neutrophil receptor, locked the cells into a night‑like, permissive state and reduced tissue damage in experimental models. The paper outlines a therapeutic route that modulates neutrophil activity temporally rather than depleting or broadly suppressing these cells, which can compromise host defenses. The authors propose ATI2341‑style approaches could limit ischemic injury without increasing infection risk, but translation will require rigorous safety and timing studies in humans.