Mechanistically, we found that PDLIM2 was repressed in the AECs of COVID-19 patients, associating with increased NF-κB, STAT3, cell cycle checkpoints, senescence, clathrin-mediated endocytosis (CME), and pro-inflammatory cytokines but decreased RhoGDI and PPAR signaling pathways (Fig. 8). This evidence concerns the gene NFKB1 and COVID-19.