Indeed, during the acute phase of the infection, an imbalanced response of types 1 and 2 T helper cells may lead to a hyperinflammatory response (35, 36), resulting in an excessive release of cytokines: in particular, higher levels of interleukin-1β (IL-1β), interleukin-6, interferon-γ, tumor necrosis factor (TNF), macrophage inflammatory protein, and vascular endothelial growth factor (VEGF) have been described in patients affected by severe COVID-19 (16–18), and are independently associated with a severe course of the infection and eventually death (16, 37). Here, IL1B is linked to infection.