In particular, a shift from an anti-inflammatory M2 type to an excessive monocyte-macrophage activation is associated to respiratory failure in severe COVID-19 patients [88] (Figure 5), characterized by subsets of mixed M1/M2 macrophage, higher expression of CD80 and CD206 and secretion of IL-6, IL-10, TNF-α, compared to controls [88]. This evidence concerns the gene IL10 and COVID-19.