The mammalian cochlea is a gem often overlooked by developmental biologists. Highly complex in function, it is never-theless highly ordered in morphology. There are clear gradients along the prin-cipal axis of the organ: in length and number of the sensory hair cells; in height, orientation, and number of sensory cilia; and in width, thickness, and stiffness of the basilar membrane. These architectural features presumably reflect transient gradients of morphogenic fac-tors and may be sensitive assays for experimental manipulation of such factors. Understanding development of the co-chlea should also have a tremendous impact on public health. More than a third of us will have substantial hearing loss by old age, most of it resulting from the death of sensory hair cells. We are born with a complement of but 30,000 hair cells; like neurons, they donot regenerate, so most hearing loss is irreversible. A few laboratories are trying to understand the factors involved in hair-cell development in order to stimulate regeneration from stem cells or dedifferentiated supporting cells. Although no one underestimates the difficulty of the task, it may be the only possible strategy for recovery from most sensorineural deafness. In understanding what makes a cell become a hair cell, much of the research is directed at expression and function of transcription factors in the inner ear. Receptors for retinoic acid and thyroid hormone have received most of the at-tention, both because these are well un-derstood and because alterations in retinoic acid or thyroid hormone during development are known to cause inner ear defects. In this context, two recent papers take on particular interest. Bradley et al.(1) have used in situhybridization to understand the spatial and temporal pattern of expression of the thyroid hormone receptors (TRs) in the developing ear. Both/3forms of TR are expressed only in the cochlearportion of the inner earat embryonic day 12 (E12) in rat, whereas the a form appears in both cochlear and vestibular regions. In a study recently reported by Kelleyet al.(2) cultured explants of developing cochlea from E13-E16 in mouse and found that addi-tion of retinoic acid alters cell fate so as to produce more hair cells.