Pacher and colleagues demonstrated that PARP1-deficient mice show a reduced mortality rate in response to high doses of LPS (58), as well as in a model of septic shock induced by cecal ligation and puncture (59), and they propose that sepsis is a potential setting for the repurposing of PARP inhibitors for therapy in non-oncological diseases (60). This evidence concerns the gene PARP1 and Shock.