In this issue of Blood, Wang et al. uncover a key role for programmed death ligand 1 (PD-L1), which delays neutrophil apoptosis at the inflammatory site through activation of the PI3K-AKT survival pathway 1. Polymorphonuclear neutrophils (PMN) are the most abundant circulating leukocytes, constituting 60 to 70% of circulating white blood cells. PMN are terminally differentiated and have a short life span, but are essential for innate immunity and host defense against microbes 2. They are the first cells to migrate out of the circulation and to be massively recruited at the infection site where they recognize microbes via different receptors expressed at their cell surface, inducing engulfment of the microbe into a phagosome 3,4. Killing of microbes by PMN occurs through the release into the phagosome of highly toxic agents such as reactive oxygen species (ROS) and granule contents including myeloperoxidase, glucosidases, proteases and anti-bacterial peptides. Microbes can also be trapped and killed by neutrophil extracellular traps (NETs) 5. Many processes such as apoptosis, NETosis, autophagy, pyroptosis, necroptosis and necrosis can induce the death of neutrophils 5 , upon which they are phagocytized and eliminated by local macrophages through a process called efferocytosis, resulting in the cleaning up of the infection site. Thus, PMN are critical anti-inflammatory components of the innate immune system as their physiological role is