Emmetropization is a process that optimizes the refractive state during postnatal development through a closed-loop negative feedback system using retinal image defocus as an error signal. The retina detects defocus and its sign, and releases biochemical messengers to adjust choroidal thickness and scleral growth. However, myopia development persists despite this mechanism, suggesting an open-loop feedback system. Studies show that the emmetropic retina can distinguish between real and simulated defocus, triggering axial eye changes. In contrast, the myopic retina has reduced ability to inhibit eye growth when positive defocus is imposed. Low spatial frequency information is involved in the emmetropic response, and the retina's defocus sign detection involves comparing blue and red end-of-spectrum blur. Myopic retinas are less responsive to this process, indicating incomplete inhibition of the feedback loop. Deprivation myopia, caused by reduced retinal image quality, is an open-loop condition for emmetropization. It can be induced by diffusers or negative lenses and is associated with genetic factors. Deprivation myopia is linked to retinal dopamine levels and can be inhibited by atropine, pirenzepine, and intense light. It shares similarities with lens-induced myopia in terms of mechanisms and responses. However, both types of myopia become open-loop when full compensation of defocus is achieved, as the feedback loop is not closed. Positive lenses induce hyperopia and can inhibit eye growth, suggesting a separate inhibitory pathway. Experiments show that positive defocus can trigger growth inhibition even when image quality is poor, indicating a robust mechanism. Recovery from myopia may also be driven by the retina detecting positive defocus, though some studies suggest other factors may be involved. The inhibitory pathway of emmetropization is distinct from the growth-stimulating pathway, with different biochemical and genetic features. Choroidal thickening in response to positive defocus may be due to metabolic factors rather than a third focusing mechanism. It is associated with increased choroidal blood flow and may be influenced by hypoxia signaling pathways. Accommodation's role in emmetropization is unclear, as studies show it may not significantly affect myopia development. The retinal ON-OFF system may play a role in detecting defocus signs, with differences between emmetropes and myopes in their responses to visual cues. Understanding these mechanisms is crucial for developing effective interventions to prevent or slow myopia progression.Emmetropization is a process that optimizes the refractive state during postnatal development through a closed-loop negative feedback system using retinal image defocus as an error signal. The retina detects defocus and its sign, and releases biochemical messengers to adjust choroidal thickness and scleral growth. However, myopia development persists despite this mechanism, suggesting an open-loop feedback system. Studies show that the emmetropic retina can distinguish between real and simulated defocus, triggering axial eye changes. In contrast, the myopic retina has reduced ability to inhibit eye growth when positive defocus is imposed. Low spatial frequency information is involved in the emmetropic response, and the retina's defocus sign detection involves comparing blue and red end-of-spectrum blur. Myopic retinas are less responsive to this process, indicating incomplete inhibition of the feedback loop. Deprivation myopia, caused by reduced retinal image quality, is an open-loop condition for emmetropization. It can be induced by diffusers or negative lenses and is associated with genetic factors. Deprivation myopia is linked to retinal dopamine levels and can be inhibited by atropine, pirenzepine, and intense light. It shares similarities with lens-induced myopia in terms of mechanisms and responses. However, both types of myopia become open-loop when full compensation of defocus is achieved, as the feedback loop is not closed. Positive lenses induce hyperopia and can inhibit eye growth, suggesting a separate inhibitory pathway. Experiments show that positive defocus can trigger growth inhibition even when image quality is poor, indicating a robust mechanism. Recovery from myopia may also be driven by the retina detecting positive defocus, though some studies suggest other factors may be involved. The inhibitory pathway of emmetropization is distinct from the growth-stimulating pathway, with different biochemical and genetic features. Choroidal thickening in response to positive defocus may be due to metabolic factors rather than a third focusing mechanism. It is associated with increased choroidal blood flow and may be influenced by hypoxia signaling pathways. Accommodation's role in emmetropization is unclear, as studies show it may not significantly affect myopia development. The retinal ON-OFF system may play a role in detecting defocus signs, with differences between emmetropes and myopes in their responses to visual cues. Understanding these mechanisms is crucial for developing effective interventions to prevent or slow myopia progression.