In all three infections, the peak in CXCR3 expression also coincided with peak expression of Treg effector molecules such as the ectonucleotidase CD39, the receptor CD103, which is expressed on activated and highly suppressive Treg cells (30), and the co-inhibitory receptors CTLA-4 and PD-1, which have also been shown to promote the suppressive function of Treg cells (31, 32) (Figure 1E). The gene discussed is CXCR3; the disease is infection.