This function of AMs is crucial as evidenced by the development of hereditary PAP in patients and mice lacking AMs due to deficiencies in either CSF2 (GMCSF) or Csf2r[206], [207] and idiopathic PAP in patients with non-functional AMs due to neutralizing auto-antibodies against CSF2 [208]. The gene discussed is CSF2; the disease is pulmonary alveolar proteinosis.