Autoimmune pulmonary alveolar proteinosis (PAP) (aPAP) is characterized by the accumulation of phospholipids and surfactant proteins in the peripheral air spaces due to alveolar macrophage dysfunction caused by anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibodies (GMAb) [1,2]. Here, CSF2 is linked to pulmonary alveolar proteinosis.