On the other hand, GM-CSF-deficient mice have relatively normal myelopoiesis with abnormal lung histology that is indistinguishable from human pulmonary alveolar proteinosis (PAP) [5], indicating a redundant role of GM-CSF in myeloid cell development and its differentiation and critical roles in the maturation and surfactant catabolism of alveolar macrophages [6]. Here, CSF2 is linked to pulmonary alveolar proteinosis.