Cytokines such as Tumor necrosis factor alpha (TNF-α), Interferons (IFN), T cells, and upregulation proteins, however, are successful in creating chronic pro-inflammatory responses in the lung parenchyma necessary to maintain granulomas in the lungs that wall off the pathogen to further spread, leading to a “latent” infection [11]. The gene discussed is IFNA1; the disease is infection.