Reduced PPARγ nuclear protein and gene expression has been demonstrated in dermal fibroblasts and in lung and skin biopsies from patients with SSc [6, 7], and in alveolar macrophages of patients with sarcoidosis and pulmonary alveolar proteinosis [4, 8], suggesting that insufficient PPARγ activity may contribute to ongoing dysregulated inflammation and fibrosis. Here, PPARG is linked to pulmonary alveolar proteinosis.