In sepsis, mitochondrial injury is possible through various conditions, including reactive nitrogen/oxygen species, overwhelming mitophagy, and impaired mitochondrial membrane permeabilization, while the exposure of mtDNA in the cytosol enhances inflammation by triggering several main signaling pathways, including toll-like receptors (TLR), NOD-like receptors, and cGAS [32]. This evidence concerns the gene CGAS and Sepsis.