Recent studies suggest that mitochondrial ROS is required for NLRP3 inflammasome activation.41, 42, 43 Moreover, many studies have indicated that mitochondrial damage and oxidative stress are important risk factors for DCM and that mitochondrial ROS is a pivotal link between oxidative stress and NLRP3 inflammasome activation.44, 45 Recently, a study has shown that monocytes and/or MDMs from T2D or DCM patients stimulated with DAMP release an elevated level of ROS.18 Meanwhile, ROS inhibitors dramatically inhibit the secretion of mature IL‐1β and IL‐18. This evidence concerns the gene NLRP3 and familial dilated cardiomyopathy.