These data lead us therefore to speculate that loss of the SH3TC2–Rab11 interaction, as a consequence of CMT4C-associated pathogenic mutations, could cause aberrant endocytic recycling of integrin-α6/β4, leading to the loss of attachment between the Schwann cell abaxonal membrane and the extracellular matrix, resulting in the destabilization of the myelin sheath and, eventually, the demyelinating peripheral neuropathy that characterizes CMT4C. The gene discussed is SH3TC2; the disease is demyelinating polyneuropathy.