Because activin A is intrinsically elevated in PPARγ deficient GM-CSF knockout mice but severely decreased in PPARγ deficient human PAP patients [16], it appeared unlikely that PPARγ would exert a direct effect on activin A. Observations made elsewhere [24] also found no evidence of a PPARγ effect on activin A. We have shown, however, that IFNγ is elevated in macrophage-specific PPARγ knockout mice and significantly reduced after in vivo restoration of PPARγ via a lentivirus vector [25]. Here, IFNG is linked to pulmonary alveolar proteinosis.