Neutrophils are the most abundant population of leukocytes, which constitute the defense again pathogens. Released by neutrophils the proteolytic enzymes and reactive oxygen species help eliminating infections, but also cause extensive tissue damage. Neutrophil apoptosis plays an esse tial role in cell homeostasis and resolution of inflammation. It is mediated by a complex network intracellular apoptotic/survival signaling pathways and can be modulated by a variety of extrace lular stimuli such as hypoxia. Here, we review recent studies on the mechanisms of neutrophil dea and survival accentuating on neutrophil apoptosis under hypoxic conditions. Neutrophils posse components of both extrinsic and intrinsic apoptotic routes. However, in neutrophils this mechanis has special features. The involvement of death receptors, caspases, mitochondria, and Bcl-2 protei are discussed. Both the transcription factor NF-кB and p38MAPK regulate the neutrophil apoptot program. Despite that reactive oxygen species (ROS) can directly promote and/or adjust apoptosi there is no consensus about the role of ROS on neutrophil lifespan. Thus both the type of RO involved and the site of their generation may be important for neutrophil apoptosis. Finally, hypox can activate several signaling pathways. The possible differences between the effects of sustain and intermittent hypoxia are also addressed.