As they grow up, approximately 25% of children in the United States become myopic (nearsighted)(Sperduto and others 1983). A much smaller percentage become significantly hyperopic (farsighted), and the majority develop little or no refractive error and thus are" emmetropic"(Sorsby and others 1957; Stenstrom 1948; Stromberg 1936). The causes of refractive error, especially myopia, have been the subject of debate for more than a century. Some have held that myopia is primarily an inherited disorder (Sorsby and others 1962; Steiger 1913; Zadnik 1997) and others, that myopia is caused by protracted near work (Donders 1864), especially by accommodation during protracted near work (Sato 1957; Young 1965). It has not been possible, based solely on clinical observations, to resolve the relative roles of heredity versus environment in the development of refractive error. In the mid-1970s, several animal models were developed to study the mechanisms underlying refractive error. Using animal models, it was found that the visual environment exerts a powerful influence on refractive state by controlling the axial length of the eye during the postnatal developmental period. Although several species have been examined, three have emerged as primary models and have played complementary roles: chick (Wallman and others 1978b), tree shrew (Sherman and others 1977), and monkey (Wiesel and Raviola 1977). Each model has advantages and disadvantages. Collectively, research on animal models has provided evidence on three specific questions:(1) Can the visual environment produce refractive error?(2) Is there an" emmetropization" mechanism that normally guides eyes to low refractive error?(3) Does excessive accommodation cause myopia? In addition, the two decades of research on animal models have provided criteria that may be used to evaluate the usefulness of particular species as models for emmetropization.