LECT2 (leukocyte cell-derived chemotaxin-2), also known as Chondromodulin-II, is a neutrophil chemotactic protein predominantly expressed in the liver (1). It was first identified in the heparin-binding components extracted from fetal bovine epiphyseal cartilage (2). Human LECT2 cDNA encodes a 151 amino acid (aa) precursor that includes an 18 aa signal sequence (3). The mature human LECT2 is a 16 kDa secreted hepatic protein that has a putative peptidase-M23 domain (3, 4). Human LECT2 shares 87% and 86% aa sequence identity with mouse and rat LECT2, respectively. LECT2 stimulates the growth and matrix formation of chondrocytes in vitro (2, 5, 6). In MC3T3-E1 cells, it promotes proliferation but inhibits alkaline phosphatase activity (5, 6). In vivo study suggested LECT2 can directly suppress the development of type II collagen antibody–induced arthritis (4). Recent studies have shown that LECT2 is an important regulator of tumor growth during hepatocellular carcinoma development and progression; it inhibits the angiogenic effect of HUVECs in vitro and in vivo (7).