Studies in inducible podocyte-specific APOL1-RA transgenic mice also showed that APOL1-G1 interferes with intracellular vesicular trafficking by impairing endocytic, autophagic and acidification pathways, as well as by disrupting the maturation of autophagosomes and autophagic flux, which correlated with the development of FSGS (Fu et al., 2017a). This evidence concerns the gene APOL1 and focal segmental glomerulosclerosis.