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. This evidence concerns the gene ENTPD1 and COVID-19.