On the other hand, studies have revealed that C/EBPβ is the regulatory link between granulocyte macrophage-colony stimulating factor (GM-CSF) signaling pathways and that C/EBPβ-deficient macrophages exhibit serious impaired proliferation of these cells [25], in which this complex stimulates fatty acid absorption and fat cell differentiation, and defective lipid metabolism is the primary cause of lung disease (PAP) and atherosclerosis. This evidence concerns the gene CSF2 and pulmonary alveolar proteinosis.