FOXP3 and neoplasm: Previous animal studies have revealed that Tregs could contribute to neovascularization through several mechanisms, including suppression of effector T cells and induction of chemokine CCL28 expression.[9,31] In a previous clinical study, the author also observed a positive correlation between tumor-infiltrating Tregs and microvessel density in HCC.[32] However, in our clinical HCC cohort, we could not validate the association between FoxP3+ cells and iMVD.