The cardiotoxicity associated with DIC limits the clinical use of doxorubicin in treating malignant tumors.[4] Several studies have reported potential molecular mechanisms of DIC, including transcriptional dysregulation mediated by topoisomerase IIβ (Top2b) inhibition, disruptions in calcium ion handling, mitochondrial iron accumulation, mitochondrial dysfunction, and alteration of cell death pathways.[5, 6] DOX accumulates in the nuclei and mitochondria of cardiomyocytes, leading to mitochondrial iron overload and excessive oxidative stress. This evidence concerns the gene TOP2B and cancer.