Although our studies using K. pneumoniae in Smart-17A mice revealed activation of reporter expression in both innate-like T cells and CD4+ Th17 cells, earlier studies demonstrated increased mortality in mice lacking γδ T cells but no difference in mortality in mice lacking αβT cells [22], [46], suggesting that γδ T cells may be a more important source of IL-17A during this infection. The gene discussed is IL17A; the disease is infection.