Based on these, we speculate that the presence of the hydrophilic SP genetic variants, particularly of SFTPA1 and SFTPA2, in a susceptible population contribute to a dysfunction/poor functioning of the innate immune response to avian antigen exposure, alters lung function and this in turn may contribute to the pathogenesis of HP. This evidence concerns the gene SFTPA1 and hypersensitivity pneumonitis.