Pulmonary TB (PTB)–induced systemic inflammation has been studied extensively showing high concentrations of acute phase proteins and proinflammatory cytokines including C-reactive protein (CRP), serum amyloid P component (SAP), interferon gamma (IFN-γ), interferon γ–induced protein 10 (IP-10), chemokine (C-C motif) ligand 1 (CCL1), and tumor necrosis factor alpha (TNF-α) in serum/plasma of active TB participants in comparison to other respiratory diseases, latent tuberculosis infection (LTBI), or healthy controls [13–16]. The gene discussed is TNF; the disease is tuberculosis.