Abstract: The regeneration of peripheral nervous system and central nervous system (CNS) neurons after injury remains challenging. We have come a long way since the identification of a 37 kDa protein specific for regenerating peripheral nervous system and CNS nerves (Muller et al., 1985). However, peripheral nervous system neurons still remain more regeneration compliant than CNS neurons. A few decades of scientific progress has led to the discovery of intrinsic (neuron specific) and extrinsic (environment specific) factors (Tedeschi and Bradke, 2017). These factors have become tightly ensconced in our understanding of neuronal development and adult neuroregeneration. Regenerative biology focuses on ways the damaged cells and tissues can be repaired or rejuvenated in the adult and may borrow plans from the patterns of connectivity during embryonic and early postnatal life (Levitan and Kaczmarek, 2015). Many of the molecular signals present during development are down-regulated in the adult. Transient induction of these molecules in adulthood may enable functional re-connectivity (Tomassy et al., 2010), for example, work on amblyopia has helped deduce the concept of plasticity breaks (Morishita et al., 2010), with the identification of Ly-6/neurotoxin-like protein 1 (Lynx1) as molecular break of plasticity. Lynx1 is largely absent during highly plastic phase of postnatal days P0–P5. The Lynx1 level in mice then increases and stabilizes with robust levels at age P60 in mouse leading to a near complete loss of plasticity. Lynx1 thus negatively modulates the plastic environment in the adult CNS of mice. Transient down-regulation of Lynx1 is thus an opportunity to confer a plastic environment in the adult CNS, allowing plasticity and regeneration of the axons possible. A CNS region optic nerve where regeneration of axons of the retinal ganglion cell (RGC) may be rendered permissive by this approach.