Given that previous studies have reported elevated levels of gzmA and gzmB in plasma of patients with severe sepsis [11, 12], and that gram-negative bacteria, as well as E. coli lipopolysaccharide (LPS), are potent inducers of in vitro release of both gzms [13], we sought to investigate the role of these gzms in the host response to E. coli-induced peritonitis and sepsis in vivo. The gene discussed is GZMA; the disease is Sepsis.