Indeed, knock-down of MAFB prior to SARS-CoV-2 exposure significantly reduces the expression of chemokines that stimulate fibrosis (CXCL13, CCL18) and neutrophil recruitment (various CXCL chemokines), 2 processes that are closely linked to COVID-19 severity and post–COVID-19 pulmonary sequelae (76). This evidence concerns the gene MAFB and COVID-19.