In this study using FDG mice in which Foxp3+ Treg cells can specifically be depleted, we demonstrated that CCl4-induced liver inflammation and fibrosis also drive hepatic Foxp3+ Treg expansion, suggesting that common self-antigens or damage-associated molecular patterns (DAMPs) including IL-33 released from stressed or damaged hepatocytes are likely to stimulate Treg cells to proliferate and regulate excessive inflammation and liver pathology. The gene discussed is FOXP3; the disease is fibrosis.