The mitochondrial redox systems, including thioredoxin 2 (Trx2) and peroxiredoxin 3 (Prx3), protect against DCM by regulating mitochondrial oxidative stress.[54, 55] Fe–S clusters, which are essential components of the mitochondrial respiratory chain and citrate cycle, play crucial roles in maintaining mitochondrial function and redox balance.[43, 44, 45] In this study, Fe–S cluster deficiency impaired electron transport, inducing ROS accumulation and mitochondrial dysfunction, which were restored by H2S supplementation. Here, PRDX3 is linked to familial dilated cardiomyopathy.