In our study, cleaved-caspase3 and Bax up-regulation, and Bcl-2 down-regulation were observed in the CKD group, suggesting that both apoptosis and ferroptosis contribute to chronic kidney injury progression and are responsible for pathological injury and interstitial fibrosis; however, neither CDDP nor DFO treatments altered apoptotic protein expression, although these interventions have previously shown pro- and anti-apoptotic effects, respectively [31, 32]; differences in dosing frequency, dosage, and/or experimental subjects most likely account for this discrepancy. The gene discussed is BCL2; the disease is chronic kidney disease.