Prompted by the clinical improvement these patients experienced on statin therapy and the recent observation that loss of GM-CSF signaling disrupts cholesterol homeostasis in Csf2rb−/− mice16, we examined the alveolar material accumulating in autoimmune PAP by studying total surfactant lipids (i.e., polar and neutral together) rather than just the polar lipid fraction as had been done previously5. The gene discussed is CSF2RB; the disease is autoimmune pulmonary alveolar proteinosis.