They postulated that a variety of bacterial toll-like receptor (TLR) ligands, such as peptidoglycans, lipopolysaccharide (LPS), and flagellins, are translocated through the damaged gut in chronic HIV infection and may drive immune activation (in addition to HIV viral Replication) and monocyte TF expression in this setting.48 The relevance of increased TF expression in HIV infection is underscored by the high levels of D-dimers in plasma and by the correlation between TF expression and D-dimer levels. The gene discussed is TF; the disease is HIV infectious disease.