The stimulated Toll-Like Receptors (TLRs), after infection by a pathogen, induce the activation of signal transduction cascades, which oblige the nuclear factor-κB (NF-κB) to translocate to the nucleus [44], followed by activation of interferon regulatory factors 3/7 (IRF3/7) or activator protein-1 (AP-1), which cooperate to initiate transcription of different cytokines such as alpha/beta interferon (IFN-α/β) to counteract infection [45, 46]. The gene discussed is NFKB1; the disease is infection.