As mentioned previously, the spiroquinoxaline derivative liproxstatin-1, another potent inhibitor of ferroptosis, was shown to protect against myocardial I/R injury in mice, maintaining mitochondrial structural integrity and function by reducing voltage-dependent anion channel 1 (VDAC1) levels and increasing GPX4 levels, thereby diminishing myocardial infarct size.426 Collectively, these findings provide compelling evidence supporting the potential of targeting mitochondrial lipid peroxidation and cardiac ferroptosis in the treatment of DOX-induced cardiomyopathy. This evidence concerns the gene VDAC1 and cardiomyopathy.