found that ferritin H deficiency promoted cardiomyopathy through SLC7A11‐mediated disulfidptosis, supporting a role of disulfidptosis in cardiomyopathy development.[18] Exposure to carbon quantum dots induces metabolic reprogramming and NADPH depletion by elevating ROS levels, leading to disulfidptosis and neuronal disorders.[19] The role of disulfide ptosis in many diseases has been partially characterized; however, the effects of disulfidptosis, on muscle atrophy are unknown. This evidence concerns the gene FTH1 and cardiomyopathy.