Macrophages, as significant inflammatory cells in AKI, have also been shown to secrete exosomes that alleviate endothelial dysfunction and reduce apoptosis and necrosis of renal tubular epithelial cells (TECs) in septic AKI through the neutrophil gelatinase-associated lipocalin-vascular cellular adhesion molecule-1 (NGAL-VCAM1) pathway [61]. The gene discussed is LCN2; the disease is acute kidney injury.