Our data on activated CD8+ T cells in IPF lungs indicate that at some point of IPF pathogenesis, these T cells experienced some MHC class I antigen/T‐cell receptor (TCR) interaction that served as signal 1 and together with a co‐stimulation signal 2 as well as additional inflammatory cytokine signaling to promote their activation and proliferation. The gene discussed is CD8A; the disease is idiopathic pulmonary fibrosis.