We have previously reported that the HP-inciting agent S. rectivirgula induces activation of PKD1 in alveolar epithelial cells, alveolar macrophages, and neutrophils via an MyD88-dependent pathway and that PKD1 contributes significantly to the acute and chronic pulmonary proinflammatory responses leading to Th1- and Th17-promoting milieu in the lungs, and development of HP caused by repeated S. rectivirgula inhalation (43, 57). The gene discussed is MYD88; the disease is hypersensitivity pneumonitis.