Studies using knockout mice or soluble inhibitors (INO1001, 1,7-dimethylxanthine) found that PARP1 was essential in driving the development of lung injury in response to various noxious stimuli including mechanical ventilation [29], lipopolysaccharide induced sepsis [30,31], and allergen sensitization in asthma [32-34]. This evidence concerns the gene PARP1 and Sepsis.