Multiple clinical forms of PAP have been described according to the presumed aetiology [11]: (1) idiopathic (primary) PAP, the most common form diagnosed in adults, which may be either congenital (mutations of α or β chains of the receptor for GM-CSF) or acquired (autoimmune PAP with autoantibodies targeting GM-CSF); (2) secondary PAP, resulting from conditions in which AM function is suppressed, such as immunodeficiency states, hematologic malignancies, exposure to inorganic dusts (eg, silica), or pharmacologically induced. The gene discussed is CSF2; the disease is autoimmune pulmonary alveolar proteinosis.