In BALF from patients with sarcoidosis, an increased frequency of a special phenotype of NK cells (CD56bright) with the capacity to produce high levels of TNF-α and IFN-γ was found, compared with BALF from healthy controls, and thereby has the potential to contribute to the TH1 alveolitis.6 Furthermore, it has been hypothesised that the release of IFN-γ from NK cells may stimulate TNF-α secretion from macrophages,7 further augmenting the TH1 response. This evidence concerns the gene IFNG and hypersensitivity pneumonitis.