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. Here, CD8A is linked to infection.