Mirror image systems of influence between reactive responsiveness and contact inhibition pathways might help better delineate relationships between axon and its enwrapping myelin sheath. Indeed, a single integral system of axon with its myelin might implicate close analogous forms of influence between the Schwann cell or the oligodendrocyte and its related axon in a manner specifically involving gene expression as patterns of pathobiology in either peripheral or central demyelinative disorders. Indeed, in terms of a conceptual system that would go beyond simple myelin subcomponent constituent deficiency arising from gene deletion or gene mutation, one might perhaps conceive axonal participation in terms of anomalous gene expression as referable specifically in terms of interactive pathobiologic effects of disturbed contact inhibition and disturbed reactive responsiveness of Schwann cell or oligodendrocyte with its related axon.It is perhaps in terms particularly of a structured superimposition of multiple myelin subcomponents both in peripheral nerves and also in central white matter that one might better conceptualize a strict mirror image series of pathways of analogous influence in determining particularly pathobiologic patterns of evolving peripheral neuropathy and of central white matter injury. In simple terms, a single mechanism of axonal participation that predetermines oligodendrocyte or Schwann cell reactivity or contact inhibitory influence would essentially help account for demyelination as primarily an integral expression of genetic influence implicating also axons.