This complex metabolic mechanism, having in AT a key player, could explain some early events observed in female mice subjected to experimental neuropathy (i.e., macrophages/microglia and myelin proteins strongly influenced by insulin, glucose metabolism and steroids), in which AT-mediated response appear to interfere with the physiological progression of WD and facilitate the development of chronic NeP, thus underlying a sex-dependent impact of AT on metabolic and inflammatory response after nerve injury. The gene discussed is INS; the disease is Wilson disease.