Finally, we tested the efficacy of PAD4 inhibition in our animal model of rupture prone CCA plaques in APOE-deficient animals with CCA tandem stenosis and observed a similar reduction in post-stroke NETosis as in WT animals, and PAD4 inhibition efficiently reduced inflammasome activation in CCA plaques (Fig. 3h–j). The gene discussed is PADI4; the disease is stroke disorder.