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Based on the analysis of the structure and trypanolytic activity of APOL1, it was proposed that APOLs could function as ion channels of intracellular membranes and be involved in mechanisms triggering programmed cell death. In this review, the recent finding that APOL1 and APOL3 inversely control the synthesis of phosphatidylinositol\u20104\u2010phosphate (PI(4)P) by the Golgi PI(4)\u2010kinase IIIB (PI4KB) is commented. APOL3 promotes Ca<jats:sup>2+<\/jats:sup>\u2010dependent activation of PI4KB, but due to their increased interaction with APOL3, APOL1 C\u2010terminal variants can inactivate APOL3, leading to reduction of Golgi PI(4)P synthesis. The impact of APOLs on several pathological processes that depend on Golgi PI(4)P levels is discussed. I propose that through their effect on PI4KB activity, APOLs control not only actomyosin activities related to vesicular trafficking, but also the generation and elongation of autophagosomes induced by inflammation.<\/jats:p>","DOI":"10.1111\/febs.15444","type":"journal-article","created":{"date-parts":[[2020,6,12]],"date-time":"2020-06-12T12:14:06Z","timestamp":1591964046000},"page":"360-381","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection"],"prefix":"10.1111","volume":"288","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5776-5640","authenticated-orcid":false,"given":"Etienne","family":"Pays","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Parasitology IBMM Universit\u00e9 Libre de Bruxelles Gosselies 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