A key feature of severe COVID-19 is dysregulated innate immune signaling, culminating in a high level of expression of numerous pro-inflammatory cytokines and chemokines, such as IL-6, TNF-α, and IL-1β—the so-called “cytokine storm”—as well as a lack of response from antiviral type I (α and β) and type III (λ) interferons (IFNs) (known to be the most potent natural antiviral mediators) [3,4]. This evidence concerns the gene TNF and COVID-19.