Cytokines from chronically activated CD8+ T cells are responsible for stimulating the monocyte-derived macrophages and aberrant epithelial cells that drive lung fibrosis after viral pneumonia (15, 16), so the roles of TNFSF14 in limiting contraction of activated CD8+ T lymphocytes and enhancing their lung residency (17) might mean that these adverse pulmonary sequelae would be mitigated by TNFSF14 blockade during infection. This evidence concerns the gene CD8A and viral pneumonia.