However, it increased expression levels of alarmins S100A12 and S100A9, and it decreased the expression of MHCII and ENTPD1 of CD14+ monocytes (Figure 6G), suggesting that persistent levels of SPP1 may contribute to long–COVID-19 pathologies by skewing monocytes toward a proinflammatory phenotype. The gene discussed is S100A12; the disease is COVID-19.