Regarding the modulation of the DCs function by SARS-CoV-2, studies documented that both monocyte-derived DCs from a healthy individual with COVID-19 and CD11C+ conventional dendritic cells (CDCs) derived from acute COVID-19 patients stimulated with proinflammatory cytokines failed to efficiently produce IFN-α and IFN-β [59,60]. The gene discussed is IFNB1; the disease is COVID-19.