Experimental studies have shown that sepsis leads to impaired mitochondrial structure and function, and overproduction of mitochondria-derived danger-associated molecular patterns (DAMPs) such as ROS, fragmented mitochondrial DNA (mtDNA), cardiolipin, N-formyl peptides, mitochondrial transcription factor A (TFAM), ATP, and cytochrome c, which worsen myocardial inflammation and sequential cardiomyopathy [36]. The gene discussed is TFAM; the disease is cardiomyopathy.