We also confirmed that in the in vivo hepatic tumor model, foxp3 expression was upregulated in the tumor-infiltrated lymphocytes, providing evidence that the growth advantages enjoyed by the CCL28-overexpressing tumor cells may be mediated by the same mechanism as what we have observed for the in vitro recruitment of the CD4+CD25+FOXP3+ Treg cells. This evidence concerns the gene CD4 and neoplasm.