Past research has reported that cytotoxic CD8+ T cells can be retained in airway mucosa, driven by an increase in TEM (effectory memory T) cells and impaired apoptosis of TRM (tissue-resident effectory memory T) cells, inducing lung injury, inflammation, airway remodeling, and other pathogeneses potentially correlated with complicated and severe pneumonia [9,32,33,34]. This evidence concerns the gene CD8A and susceptibility to pneumonia measurement.