The functional biology of the STM counterparts (i.e., CD48hiS100A12+ and CD48+SPP1+) showed that they were the main producers of pathogenic TNF, IL-6, IL-1β, and chemokines in the synovium of RA, and this resembles the lung hypercytokine environment characterizing severe COVID-19 respiratory distress syndrome (53, 54), suggesting that SPP1+ and S100A12+ BALF macrophage clusters might be the key source of these mediators in the COVID-19 lung. Here, IL1B is linked to newborn respiratory distress syndrome.