It is hypothesized that the dysregulation of Tumor Necrosis Factor-α/Tumor Necrosis Factor Receptor 1 signaling, upregulation of inhibitory receptors, and prolonged antigen exposure may contribute to the dysfunction observed in antigen-specific T-cell responses in COVID-19 patients with severe disease [35,37,38]. This evidence concerns the gene TNFRSF1A and COVID-19.