APOA1 and focal segmental glomerulosclerosis: Chhuon et al. [28] shed light on some potential mechanisms involved in FSGS recurrence, by comparing plasma proteomic findings (including soluble proteins and extracellular vesicle proteomic profile) of post-transplant recurrent FSGS patients to non-INS patients and healthy controls: upregulated proteins were involved in neutrophil degranulation and downregulated proteins involved in platelet degranulation and lipid-binding (including APOA1).