CSF3 and acute respiratory distress syndrome: 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).