Since single-cell transcriptomics on lungs from patients with long COVID with fibrosis has revealed a decrease in lung-resident alveolar macrophages and an increase in monocyte-derived macrophages with enhanced expression of various MAFB-dependent genes (CCL2, CCL8, CCL18, STAB1) (77), our results on the MAFB-dependent macrophage transcriptome might be also applicable to the case of lung pathogenic macrophages in long COVID. This evidence concerns the gene CCL2 and fibrosis.