Neutrophils from SLE patients also tend to undergo spontaneous NETosis, resulting in the release of LL-37, citrullinated histones, neutrophil elastase, and MPO which are attached to the NET chromatin fibers.[24,25] These further serve as autoantigens which can in turn activate plasmacytoid dendritic cells (pDCs) to produce large amounts of IFNα, thereby triggering a self-amplifying pathogenic loop.[26] Moreover, NETs can mediate cardiovascular atherosclerotic complications in SLE patients by promoting endothelial damage through activation of the endothelial MMP-2. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.