The problem and objectives Balance between cell death and proliferation is important during development, homeostasis, and immune responses. Removal of dying cells by phagocytes is critical in preventing unwanted inflammatory responses and forms an integral part of programmed cell death. Necrotic cell death, as well as delayed removal of apoptotic cells that results in secondary necrosis, leads to the release of intracellular content that can act as damage-associated molecular patterns (DAMPs), provoking inflammation through pattern recognition receptors (PRRs). Defective phagocytosis is known to be associated with pathologies such as atherosclerosis, airway inflammation, and autoimmunity. However, broader implication of phagocytosis in inflammatory diseases in general is currently unknown. Accumulating knowledge on the mechanism of apoptotic cell clearance provides us a means to address its potentially beneficial role in resolution of inflammation and tissue regeneration.