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Apolipoproteins L (APOLs) are membrane-associated proteins involved in both resistance to pathogens, such as APOL1-mediated killing of African trypanosomes or APOL3-mediated lysis of intracellular bacteria, and induction of diseases, like APOL1-mediated nephropathy or APOL2-mediated liver fibrosis. Accumulating evidence points to APOLs controlling membrane dynamics linked to immunity. APOL1 and APOL3 are induced by inflammatory signalling and play key roles in the initiation and termination of inflammation by promoting the traffic of Golgi-derived membranes involved in STING activation, as well as mitochondrial membrane fission and fusion involved in auto/mitophagy. APOL2, or murine mAPOL8, is required for profibrotic vesicle exocytosis, whereas mAPOL9 triggers bacterial membrane budding linked to gut immunity control. In dendritic cells, APOL3 or the APOL3-like mAPOL7C promote megapore formation in phagosomal membranes, allowing antigen cross-presentation and apoptosis, both probably linked to cardiolipin solubilization. In adipocytes, mAPOL6 controls inflammation-linked lipid droplets dynamics. Through their membrane-remodeling activities, APOLs participate in the control of infection by bacteria, viruses, and parasites. Thus, natural APOLs mutations represent inborn errors of immunity.