It was confirmed that IL-33 served as an “alarmin” released by stressed hepatocytes, which could bind to the receptor termed suppressor of tumorigenicity 2 (ST2), then activated NF-kB and mitogenactivated protein kinases (MAPKs) pathways, ultimately promoting the formation of liver fibrosis (100, 101). This evidence concerns the gene IL1RL1 and Hepatic fibrosis.