The authors suggested that inflammation persists in the presence of so many Tregs, probably due to the suppressed function of Tregs within the liver microenvironment, seeing that only 5%–15% of the liver-infiltrating FOXP3+ cells expressed pSTAT5, the marker of intrahepatic Tregs activation [45], and the defective function of Tregs has been implicated in PBC [44]. The gene discussed is FOXP3; the disease is primary biliary cholangitis.