The liver tumors may evade the host immunosurveillance and maintain the growth advantages by upregulating expression of CCL28 during hypoxia; and by binding to its receptor, CCR10, CCL28 can effectively recruit CCR10+ Treg cells to the tumor site, where this specific population of Treg cells repress the functions of effector T-cells, promoting the in vivo tumor growth. This evidence concerns the gene CCL28 and neoplasm.