Patients with severe CoV-19 infection further experience a systemic inflammatory response and acute respiratory distress syndrome (ARDS), which results from “cytokine storm syndrome” 21, an aberrant interaction among interferons, interleukins, chemokines, etc. As a result, severe COVID-19 patients express higher amounts of proinflammatory cytokines, including interleukin (IL)-6, IL-10, IL-1β, monocyte chemoattractant protein 1 (MCP1) and tumor necrosis factor (TNF)-α 22, 23. This evidence concerns the gene CCL2 and COVID-19.