Targeting the release of histone complexes and, in particular, inhibiting NETosis has demonstrated considerable specificity and efficacy when used in animal models of AOI55, 56, 60 and sepsis.101 Specific PAD4 inhibitors prevent the citrullination of H3, a key step in releasing nucleosomic material for NET formation,102 and are more effective than DNase1 in preventing tissue damage.103 DNase1 theoretically disperses DNA-bound-histone, and hence, reduced NET-mediated cytotoxicity.55 but are unlikely to be able to effectively access DNase1 binding sites within multifarious NET complexes. The gene discussed is DNASE1; the disease is Sepsis.