Consistent with previous findings that genetic deletion of Ctsl led to an attenuation of pancreatitis (43), atherosclerosis (44), intimal hyperplasia (45), and antigen-induced arthritis (46), we found that genetic disruption of pCTS-L similarly lessened CLP-induced injury to the liver (Fig. 7C), confirming a pathogenic role of pCTS-L in lethal sepsis. Here, CTSL is linked to pancreatitis.