CCL18 and COVID-19: Since MAFB silencing before GSK3β-inhibition in M-MØ (Supplemental Figure 2, E and F) impaired the enhanced expression of MAFB-dependent genes (Figure 2G) as well as the increased secretion of the profibrotic factors LGMN, CCL18, and IL-10 provoked by GSK3β-inhibition (Figure 2H), we could conclude that MAFB mediates the macrophage reprogramming action of GSK3β and the potentiating effect that GSK3β-inhibition has on the gene sets that characterize pathogenic macrophage subsets in severe COVID-19.