During the process of septic response, activated KCs release leukotriene B4 and TNF-α, which in turn attract blood neutrophils into the liver and activate them.[16] Apoptotic hepatocytes have also been shown to function as chemotactic signals, triggering neutrophil transmigration.[17] Upregulation of endothelial integrins and intercellular adhesion molecule (ICAM)-1 also promotes neutrophil migration in LPS-induced liver injury.[18] In contrast, heme oxygenase (HO)-1 in neutrophil attenuates its infiltration in liver during sepsis via the inactivation of p38 MAPK. The gene discussed is HMOX1; the disease is Sepsis.