In summary, the identification of MAFB-dependent genes and functions in human monocyte–derived macrophages, which become the major pulmonary macrophage population during COVID-19, has shown that MAFB shapes the macrophage transcriptome under both basal and virus-stimulated conditions; it also demonstrates that MAFB mediates the acquisition of the proinflammatory and profibrotic profile of pathogenic macrophages in severe COVID-19 and regulates the production of chemokines implicated in neutrophil recruitment, a driving factor for post-COVID-19 interstitial lung disease (76). The gene discussed is MAFB; the disease is interstitial lung disease.