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In the lungs, after entering in type II alveolar cells, SARS-CoV-2 infected cells become defective for surfactant production (Ghati et al., 2021) and release cytokines, like IL-8 among others, which in turn activate alveolar macrophages to release IL-1, IL-6, and TNF-α, that induce natural killer and dendritic cell differentiation and macrophage M1 polarization, enhancing the proinflammatory response with increased vasodilation causing neutrophil and activated T cell influx from the capillaries into the alveolus, all leading to the cytokine storm (Figure 2)