CGAS and Sepsis: This includes sensing circulating bacterial and viral pathogens that will interact with the endothelium and initiate the innate immune response, which when systemic can lead to the development of sepsis.34 This is certainly consistent with evidence that the bacterial endotoxin LPS induces mitochondrial DNA release into the cytosol of ECs that activates cGAS.32 This process of cGAS activation was found to suppress EC proliferation through the downregulation of YAP1 signaling.