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The current paradigm of the pathogenesis of idiopathic pulmonary fibrosis (IPF) indicates that persistent injury to alveolar epithelial cells (AECs) results in the activation of aSMA (a-smooth muscle actin)-expressing myofibroblasts (1). Although no single mouse model fully recapitulates the human IPF disease state, the bleomycin-induced lung injury model remains the most widely accepted method of translational research despite its limitations, which include a paucity of histological findings of usual interstitial pneumonia and the lack of collagen cross-linking, resulting in reversible fibrosis (2, 3). Therapies that reverse pulmonary fibrosis remain elusive and represent a significant, unmet clinical need; we present three novel studies that highlight recent developments in IPF translational research that forges a path for an innovative approach in treating IPF through the novel application of three well-known drugs. n

New Applications of Old Drugs as Novel Therapies in Idiopathic Pulmonary Fibrosis. Metformin, Hydroxychloroquine, and Thyroid Hormone