Good visual acuity requires that the axial length of the ocular globe is matched to the refractive power of the cornea and lens in order to focus the images of distant objects onto the retina. During the growth of the juvenile eye, this is achieved through the emmetropisation process that adjusts the ocular axial length to compensate for the refractive changes that occur in the anterior segment. A failure of the emmetropisation process can result in either excessive or insufficient axial growth, leading to myopia or hyperopia, respectively. Emmetropization is mainly regulated by the retina, which generates two opposite signals: ‘GO/GROW’ signals to increase axial growth and ‘STOP’ signals to block it. The presence of ‘GO/GROW’ and 'STOP’ signals was investigated by a proteomic analysis of the retinas from chicken with experimental myopia and hyperopia. Of 18 differentially expressed proteins that were identified, 5 display an expression profile corresponding to ‘GO/GROW’ signals and 2 correspond to ‘STOP’ signals. Western blotting confirmed that Apolipoprotein A1 (Apo A1) has the characteristics of a ‘STOP’ signal both in the retina as well as in the fibrous sclera. In accordance with this, intraocular application of the PPAR-alpha agonist GW7647 resulted in upregulation of Apo A1 levels and in a significant reduction of experimental myopia. In conclusion, using a comprehensive functional proteomics analysis of chicken ocular growth models we identified targets for ocular growth control. The correlation of elevated ApoA1 levels with reduced ocular axial growth points towards a functional relationship with the observed morphological changes of the eye.