Prior reports have demonstrated infiltrates of Treg in both human and murine PDA based on immunohistochemical detection of FOXP3, the transcription factor that is critical for Treg development and function.[11], [13] Consistent with these studies, we routinely detected populations of CD4+ Treg (CD25+FOXP3+CD127−) in the single cell suspensions prepared from human PDA, and the proportion of Treg among CD4+ T cells in the tumor microenvironment was significantly higher than in the blood (p<0.0001; Figure 3C). The gene discussed is FOXP3; the disease is Patent ductus arteriosus.