Simonian et al. demonstrated that, in a Bacillus subtilis-induced HP model, IL-17 expressed by γδ T cells play a role in bacterial clearance and downregulate inflammatory responses and lung fibrosis [25, 26], whereas in another Saccharopolyspora rectivirgula-induced HP model, IL-17 expressed by CD4+ T cells, which acted as a proinflammatory cytokine, produced an unregulated inflammatory and fibrotic response and promoted rather than protect against hypersensitivity pneumonitis and lung fibrosis [7]. The gene discussed is IL17A; the disease is hypersensitivity pneumonitis.