Furthermore, our study demonstrated that IMD1-53 protected against atherosclerosis and stabilized the lesions by inhibiting ERS-C/EBP-homologous protein- (CHOP-) mediated macrophage apoptosis, and the subsequent NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome triggered inflammation [90, 91]. Here, DDIT3 is linked to atherosclerosis.