Upon infection, M. pneumoniae attaches to bronchial epithelial cells via surface-exposed adhesins, which trigger a series of cascade reactions involving interactions with toll-like receptors (TLR1, TLR2, and TLR6) [6], mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), and activated protein-1 (AP-1), leading to the production of diverse pro-inflammatory cytokines and inflammatory mediators [7–9]. The gene discussed is TLR2; the disease is infection.