Optic nerve atrophy is not an isolated disease; any irreversible damage caused to the retinal ganglion cells and their axons can lead to the development of the disease; therefore, it is a pathological diagnosis, but it is misnamed as a diagnostic term by domestic and international clinics. It is a misconception that clinicians often judge severe visual impairment by the pale or white color of the optic disc, because the pale or white color of the optic disc only indicates atrophy of the optic disc capillaries or proliferation of glial cells resulting in enhanced reflection and loss of redness, but does not indicate severe damage to the optic nerve fibers and visual function [1]. It is just as hasty to determine that an emergency patient with “no light perception” ocular trauma will be permanently blind, as it is common to see substantial improvement in visual acuity after surgery or with medication. Clinical cases of optic nerve atrophy patients with pale optic discs and 1.0 visual acuity are common. However, the message most physicians send to their patients is “no hope for treatment”, resulting in many patients being deprived of reasonable treatment or losing the opportunity for treatment. Recent studies have found that as long as a small number of nerve cells survive in the damaged structure, recovery of function is possible. The compensatory capacity of optic nerve fibers is very strong, 40-50% of the nerve fibers can reach 1.0 vision, 11% of the nerve fibers can reach 0.5 vision, 5% of the nerve fibers can reach 0.1 vision, therefore, it is significant to actively maintain the function of the residual nerve fibers. It is important not to wait for this small percentage of “hardy” nerve fibers to be depleted before seeking treatment. Retinal thinning, especially in the macula, does not mean that visual function is severely impaired. Studies have found that only when retinal thickness decreases to 70-80 μm, or when nerve fiber damage reaches 40% or more in glaucoma patients, does significant visual field loss occur, often preceded by a decrease in contrast sensitivity and color sensitivity. Therefore, it is also hasty to judge the poor prognosis of visual function by finding retinal thinning by imaging (e.g., OCT). So why is it difficult for optic nerve damage areas to activate and repair themselves in patients with optic nerve atrophy in daily life? This is because patients tend to focus their attention on the “undamaged” sector of the visual field in daily life, and the residual visual structures lack sufficient attentional resources, leading to a reduced activation state and a limitation of simultaneous physiological repair. From a pathological point of view, we can classify the nerve fibers of patients with optic nerve atrophy into three categories: completely dead nerve fibers, dying or threatened nerve fibers, and normal nerve fibers. This is the key to saving and treating optic nerve atrophy. Not only do the dying or threatened nerve fibers themselves cause loss of visual function, but the toxic components of their breakdown (e.g., oxygen radicals, glutamate, nitric oxide) can directly damage normal nerve fibers, which may partially explain why visual function is still quietly impaired after the causative factors (e.g., high intraocular pressure, inflammation, edema, vascular obstruction, silicone oil filling, etc.) are eliminated. This is one of the reasons why it is important to actively eliminate the causative cause early, avoid secondary damage, and actively salvage this part of the fiber function. In terms of treatment, it is very important to promote nerve fiber repair and functional recovery. It is much more important to promote the whole body and systemic repair than to target a certain part of the treatment (e.g., nutritional support, improvement of microcirculation). Neurotrophic drugs (e.g., vitamins, neurotrophic factors) are only effective for patients with optic nerve atrophy caused by nutritional deficiencies (e.g., vitamin B1 deficiency, vitamin B12 deficiency, pernicious anemia, tobacco and alcohol intoxication), but most patients with optic nerve atrophy have a comprehensive, multifaceted, and optimally proportioned “nutrients” that are locally deficient. However, the majority of optic nerve atrophy patients lack a comprehensive, multifaceted, and optimally proportioned “nutrients”, not just vitamins and neurotrophic factors. Therefore, clinicians should not “see the trees but not the forest”. Optic nerve atrophy is often a manifestation of the organic imbalance in the eye, and if we can restore the balance of the body and improve the mental condition, then the repair of local nerve fibers must be beneficial. The “residual visual activation theory” is a new concept introduced in 2011, which has brought the treatment of optic nerve atrophy to a new stage. Although nerve fiber damage is irreversible, it can be compensated or reconstructed, especially in posterior visual pathways, such as cortical blindness, which can form a bypass or initiate a potential visual pathway in later stages. Some visual function has been shown to be restored, improved, or stabilized by tapping into residual visual function, including various low vision rehabilitation techniques, medications (including herbal medicine), and by appropriate stimulation of the partially damaged visual system (e.g., visual physical examinations, visual training, current stimulation, grating stimulation of the visual field junction area, etc.) [2]. This is true for vascular obstruction, ischemia, trauma, glaucoma, drug toxicity, as well as advanced uveitis, pathological myopia, retinitis pigmentosa, and hereditary optic neuropathy. Given that early cerebral infarction patients should undergo rehabilitation as early as possible after the acute onset, the Neuro-Ophthalmology Group of the Chinese Medical Association Ophthalmology Branch also advocates that early visual function training is beneficial for patients with optic neuropathy. In summary, clinicians should avoid simply pessimizing optic nerve atrophy as an incurable, independent disease and should instead adopt a comprehensive diagnostic and management strategy. In a patient with poor visual acuity, every small improvement in visual function has a more significant improvement in his/her quality of life, such as “0.1 → 0.2” or even “manual → several fingers”, which is much more significant in improving the patient’s quality of life than “0.8 → 1.0”. It is the responsibility and obligation of contemporary neuro-ophthalmologists to do their best to save or stabilize the residual visual function of patients, and it is the goal of every ophthalmologist to pursue “useful vision in the lifetime” of patients with optic nerve atrophy.