FOXP3 and neoplasm: Again, these immunoregulatory effects can result in being detrimental in the course of chronic infections or tumors, because FOXP3+ Tregs acquire strong suppression capacity in these contexts, through various signals (e.g., by interaction between OX40L expressed on tumor-associated macrophages and OX40 delivering survival signals in Tregs) favoring demethylation of the Treg-specific demethylated region that acts as a transcriptional stabilizer of FOXP3 gene and consequent suppression function [as reviewed in (70, 79)].