This is an important finding because an increased PD-L1 expression in mononuclear phagocytes is associated with the inhibition of T cell proliferation and IFN-g in the context of TB, the PD-1/PD-L1 pathway inhibits T cell effector functions during TB, and a high PD-L1/CD86 ratio is part of the CD16+/CD163+/MerTK+/PD-L1/pSTAT3+ signature in MFs that are susceptible to Mtb infection, and possess immunosuppressive activity toward the Th1 response (Lastrucci et al. 2015). The gene discussed is CD86; the disease is tuberculosis.