Later studies confirmed that the sugar moiety of PGL is unique in its capacity to bind the lectin domain of CR3 for efficient infection of human macrophages, and M. tuberculosis PGLs are able to inhibit Toll-like receptor 2-triggered NF-κB activation and thus the pro-inflammatory response, thus assisting M. tuberculosis to subvert the host immune response (145) (Table 1). The gene discussed is CRIPTO3; the disease is infection.