Cisplatin exposure leads to mtDNA leakage and activation of the cGAS‐STING pathway, thereby aggravating renal inflammation and AKI progression.[49] Cisplatin binding to mtDNA is also proposed to prevent mitochondrial DNA replication and transcription, resulting in an imbalance in mitochondrial proteomics and subsequent mitochondrial damage, as suggested by mitochondrial ROS burst, mitochondrial fragmentation, the reduction in mitochondrial cristae, mitochondrial depolarization, and reduced ATP production. The gene discussed is STING1; the disease is acute kidney injury.