PAP has been described in three forms clinically: primary PAP that can be autoimmune PAP which is associated with elevated levels of autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF) or hereditary PAP which is due to gene mutations of GM-CSF receptor alpha and beta genes (CSF2RA and CSF2RB, respectively), secondary PAP, and congenital PAP. Here, CSF2 is linked to autoimmune pulmonary alveolar proteinosis.