The pathophysiological mechanisms underlying SARS-CoV-2 infection involve the activation of a cytokine storm in the lung with recruitment of a number of cytokines, chemokines, and growth factors, such as IL-1β, IL-2, IL-6, IL-8, G-CSF, IP-10, MCP-1, MIP-1α, MIP-1β, IFN-γ, and TNF-α, followed by lung edema, impairment of air exchange, and acute respiratory distress syndrome, which in turn leads to secondary infection, multiple organ failure, and eventually death (3, 37, 38). Here, CCL3 is linked to acute respiratory distress syndrome.