The reasons for the increase of procalcitonin concentration may be on the one hand, the intestinal barrier of patients with liver cirrhosis or liver failure was damaged, and the intestinal bacteria were ectopic, which led to endotoxemia and the increase of PCT synthesis; on the other hand, the damage, apoptosis, or necrosis of hepatocytes resulted in the release of damage-associated molecular patterns (DAMPS), activated the downstream pathways including IL-1β and TNF-α, and stimulated the expression of PCT [16, 31]. This evidence concerns the gene IL1B and liver failure.