Transplantation of AMs as well as Csf2rb2-sufficient Mφ progenitors (fetal liver monocytes, yolk-sac Mφs and BM monocytes) has been shown to be sufficient to prevent PAP development in Csf2rb2-/- mice [13], [209], further highlighting the essential role played by AMs in PAP progression and providing a potential new therapy option for this disease. This evidence concerns the gene CSF2RBP1 and pulmonary alveolar proteinosis.