This effect decreased in the presence of the endocytosis inhibitor cytochalasin D (372.30 ± 11.02 versus 213.80 ± 9.97 ng/ml, P < 0.005, Fig. 2C) and the vacuolar type H+-ATPase inhibitor bafilomycin A1 (219.42 ± 10.68 ng/ml, P < 0.005), suggesting that SLE pEVs induced NETs formation by uptake and activation of endolysosomal Toll-like receptors (e.g., TLR3, 7, 8 and 9). This evidence concerns the gene ATP6V1A and systemic lupus erythematosus.