In this regard, Warnatsch et al. demonstrated the consequences of targeting NETs in the pathogenesis of atherosclerosis by observing diminished atherosclerotic lesion size, lower systemic IL-1β levels and decreased NETosis ratios in HFD-fed, Apo-E-deficient and LDL-deficient mice when they lack the expression of the neutrophil proteases NE or PR3 [145]. Here, IL1B is linked to atherosclerosis.