As the basic gas-exchange units of the lung, alveoli must be elastic (to allow expansion and contraction with respiration) and thin (to facilitate gas exchange with the capillary network). Alveolar walls are among the most delicate structures in the vertebrate body, yet they are in constant contact with the external environment (inspired air) and undergo tens of thousands of cycles of inflation each day. Nonetheless, most evidence indicates that alveoli are relatively durable. Alveolization, or the formation of alveoli during lung development, is essentially completed in the neonatal period, and little neo-alveolization occurs in the adult lung. Despite their normal durability, damage to alveolar walls is a root cause of diseases such as emphysema and results in loss of functional gas-exchange capacity, as well as impairing lung mechanics. In premature neonates of very low birth weight, whose lungs are structurally or morphologically immature, alveolization may be impaired, resulting in poor lung function. Therapies capable of promoting alveolization are therefore of great interest. Until recently, there has been little basis for optimism about therapeutic measures to promote alveolization, either in the premature neonatal lung or in the emphysematous lung. However, it has long been known that vitamin A is essential for normal lung epithelial cell homeostasis. Several studies have shown that retinoids are effective in promoting alveolization in neonatal rats (1), in adult rats with elastase-induced emphysema (2), and in mice with a genetic defect (Tsk) involving impaired alveolar development (3). Vitamin A supplementation has been explored as a therapy for premature infants of very low birth weight as early as 1987 (4), and based on its efficacy in promoting alveolization in animal models, it is currently being tested in clinical trials in humans. There is still much to learn about the role of retinoids in alveolization, or even about how alveolization occurs. In this issue, McGowan and coworkers report that elastin expression by alveolar myofibroblasts is specifically regulated by retinoid treatment in the developing lung, and that specific retinoid receptor subtypes are important for both normal alveolization and normal elastin expression in the neonatal lung (5). These and other emerging reports of retinoid-responsive genes in the developing lung form a new body of data that may lead to more specific treatments to enhance alveolization.