Moreover, conversion of arginine to citrulline on histones by peptidyl arginine deiminase 4 (PAD4) is necessary to promote chromatin decondensation and the subsequent release of NETs in the extracellular environment.21 Interestingly, pharmacological or genetic inhibition of PAD4 disrupts NET release and reduces pathology in various murine disease models, including atherosclerosis,22 inflammatory arthritis (IA),23 and SLE.24,25 Therefore, NETs are potential therapeutic targets for different acute and chronic inflammatory disorders. This evidence concerns the gene PADI4 and atherosclerosis.