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. The gene discussed is CEBPB; the disease is pulmonary alveolar proteinosis.