In TB, defective activation of myeloid cells8,13 may contribute to impaired TB immunity by suppression of Th1 effector cells and activation of different pathogenic and Treg cell subsets with a large phenotypic and functional heterogeneity, including expression of immune checkpoint molecules, such as IDO, cytotoxic T-lymphocyte-associated protein (CTLA)-4, programmed death ligand (PD-L)1, and LAG-3.14 The gene discussed is CTLA4; the disease is tuberculosis.