The mammalian respiratory system is responsible for gas exchange, making it vulnerable to injury from inhaled pollutants or respiratory viruses; yet the mechanisms that promote tissue repair to preserve adult airway integrity have remained poorly understood. The Hedgehog (Hh) signaling pathway governs embryonic development and adult tissue homeostasis. In organs like the mouse urinary bladder, epithelium-derived Hh signals trigger a feedback response from stromal cells to regulate epithelial homeostasis and repair. To investigate the involvement of Hh signaling in adult tracheal airway repair, the authors examined the steady-state expression of Hh ligands. Surprisingly, among the three Hh family members, only Dhh exhibited detectable expression by RNA-seq, whereas Sonic hedgehog (Shh) and Indian hedgehog (Ihh) were undetectable. Importantly, the expression of a pathway reporter Gli1 -- encoding a member of the Gli-family of Hh pathway transcription factors -- in stromal cells was diminished in Dhh mice, suggesting that Dhh is the major Hh ligand responsible for activating Gli1 in adult tracheal airway. To determine whether Dhh is essential for airway regeneration after injury, the authors examined mice subjected to inhalation of SO, which induces damage of proximal airway epithelial cells. They found that 1) SO caused more dramatic epithelial damage in Dhh mice than in control mice, and 2) Gli1 mice suffered severe epithelial damage like Dhh mice, suggesting that Dhh promotes airway epithelial repair through Gli1.