The local proliferation of AMs is primarily dependent on GM-CSF, and GM-CSF-deficient mice have shown multiple adverse effects in AMs including phagocytosis, cell adhesion, surface receptor expression (TLR and mannose receptor), and surfactant catabolism mediated by the PU.1 transcription factor, resulting in alveolar proteinosis and increased susceptibility to respiratory infections [102]. Here, CSF2 is linked to Intraalveolar phospholipid accumulation.