In vitro and in vivo studies using preclinical sepsis models demonstrated that sepsis triggers impairments in the structure and function of mitochondria, which abnormality leads to not only a deficiency in energy supply but also an overproduction of mitochondria-derived danger-associated molecular patterns (DAMPs), such as reactive oxygen species (mtROS) [14], fragmented mitochondrial DNA (mtDNA) [15,16,17,18], N-formyl peptides [19], cardiolipin [20], ATP [21], mitochondrial transcription factor A [22], and cytochrome c [23]. This evidence concerns the gene TFAM and Sepsis.