Current Neuroscience dogma holds that transections or ablations of a segment of peripheral nerves produce:(1) Immediate loss of axonal continuity,sensory signaling,and motor control;(2) Wallerian rapid (1-3 days) degeneration of severed distal axons,muscle atrophy,and poor behavioral recovery after many months (if ever,after ablations) by slowly-regenerating (1 mm/d),proximal-stump outgrowths that must specifically reinnervate denervated targets;(3) Poor acceptance of microsutured nerve allografts,even if tissue-matched and immune-suppressed.Repair of transections/ablations by neurorrhaphy and well-specified-sequences of PEG-fusion solutions (one containing polyethylene glycol,PEG) successfully address these problems.However,conundrums and confusions regarding unorthodox and dramatic results of PEG-fusion repair in animal model systems often lead to misunderstandings.For example,(1) Axonal continuity and signaling is re-established within minutes by non-specifically PEG-fusing (connecting) severed motor and sensory axons across each lesion site,but remarkable behavioral recovery to near-unoperated levels takes several weeks;(2) Many distal stumps of inappropriately-reconnected,PEG-fused axons do not ever (Wallerian) degenerate and continuously innervate muscle fibers that undergo much less atrophy than otherwise-denervated muscle fibers;(3) Host rats do not reject PEG-fused donor nerve allografts in a non-immuno-privileged environment with no tissue matching or immunosuppression;(4) PEG fuses apposed open axonal ends or seals each shut (thereby preventing PEG-fusion),depending on the experimental protocol;(5) PEG-fusion protocols produce similar results in animal model systems and early human case studies.Hence,iconoclastic PEG-fusion data appropriately understood might provoke a re-thinking of some Neuroscience dogma and a paradigm shift in clinical treatment of peripheral nerve injuries.