It has been suggested that emmetropic and low-hyperopic eyes in which the refractive error in the periphery of the visual field is relatively hyperopic with respect to the axial refraction may be at greater risk of developing myopia than eyes with similar refractions but relatively myopic peripheral refractive errors. The animal and human evidence to support this hypothesis is reviewed. The most persuasive studies are those in which emmetropization has been shown to occur in infant rhesus monkeys with ablated foveas but intact peripheral fields, and the demonstration that, in similar animals, lens-induced relative peripheral hyperopia produces central axial myopia. Evidence for emmetropization in animals with severed optic nerves suggests that emmetropization is primarily controlled at the retinal level but that the higher levels of the visual system play a significant role in refining the process: there appear to be no directly equivalent human studies. Since any contribution of the higher centres to the control of refractive development must depend upon the sensitivity to defocus, the results of human studies of the changes in depth-of-focus across the field and of the contribution of the retinal periphery to the accommodation response are discussed. Although peripheral resolution is relatively insensitive to focus, this is not the case for detection. Moreover accommodation occurs to peripheral stimuli out to a field angle of at least 10 deg, and the presence of a peripheral stimulus can influence the accommodation to a central target. Although the basic hypothesis that a relatively hyperopic peripheral refractive error can drive the development of human myopia remains unproven, the available data support the possibility of an interaction between the states of focus on axis and in the periphery.