The evidence that SARS-CoV-2 can cause different clinical outcomes from asymptomatic to severe symptomatic infection range, leads to hypothesize that it is a poor cytopathic virus, and cell damage is not due to a direct viral effect, but rather by the immune responses elicited to eliminate the virus-infected cells by various effector mechanisms, including killing by CD8+ T cells and NK cells, PRR-dependent activation of pro-inflammatory cells (e.g., macrophages, neutrophils...), antiviral and inflammatory cytokines produced by NK cells, NKT cells, ILCs, CD4+ and CD8+ T cells, TRM cells [42]. The gene discussed is CD8A; the disease is infection.