The current state of research into experimentally induced refractive errors is reviewed. The area is analysed in three components-the transduction of defocus or deprivation, the vector for transmitting the error message from the retina to the outer tunics of the eye, and the identity of the effector for causing growth modulation in the sclera. Anatomical, pharmacological, electrophysiological and optical factors are considered in terms of which elements of the retina are necessary to support a refractive response to deprivation or defocus. Two of the current models are discussed-one emphasizing the role of the choroid in effecting ocular and refractive change, while the second model approaches the problem from the aspect of scleral changes that are associated with growth adaptation without emphasis on the error detection mechanism. A third model is proposed in which the error signal for deprivation or defocus is detected in the outer retina and where error is translated through separate signals for stimulus brightening and darkening into a net signal for fluid flow across and under the active control of the retinal pigment epithelium with the fluid communication between the vitreous chamber and the choroidal lymphatics. The directions of research both fundamental and clinical which are needed to create pharmaceutical or environmental solutions to refractive control are discussed.