Due to activation of the TLRs pathway, dependent or not of MyD88, nuclear factor kappa-B (NF-κB) becomes activated and translocates to the nucleus [11], where it promotes transcription of specific genes, including some related to the immune response, e.g. interferon-gamma (IFN-γ), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), all mediators of inflammation [10–13], and strongly associated with the mechanism of cardiac hypertrophy [14–16]. The gene discussed is TNF; the disease is cardiac hypertrophy.