Abstract: Peripheral nerve injuries (PNI) are common following blunt or penetrating trauma and can lead to disability and chronic pain in affected individuals, with limited options available to promote regeneration and functional recovery. From animal models, it is known that the regenerative capacity of the peripheral nervous system (PNS) is heavily dependent upon the remarkable ability of Schwann cells to undergo a phenotypic shift from a supportive/myelinating/maintaining phenotype to one that encourages neural regeneration. In rodents, a great deal is known about the molecular signals that control this process or mark the cells and cellular changes involved (Boerboom et al., 2017; Jessen and Mirsky, 2019). Effective translation of the wealth of animal model data into a human paradigm of nerve injury would be of great benefit in the development of improved clinical treatments. However, progress has been limited by ethical and practical challenges associated with studying human nerve injury (Hewitt et al., 2008; Wilcox et al., 2019). Moreover, the intricate anatomy and diverse range of injuries make PNI a heterogeneous pathology to study. To address this issue, in our recent article entitled Characterizing cellular and molecular features of human peripheral nerve degeneration, we analyzed nerve tissue retrieved from patients undergoing reconstructive nerve procedures (Wilcox et al., 2020). Since the patients had a range of differing time intervals between injury and surgery, it was possible to construct an impression of the phenotypic changes of Schwann cells within a population over acute and chronic time points of denervation. The findings reveal novel information about the cellular and molecular features that underpin human nerve degeneration. The patterns of changes seen in the human nerve samples were similar to those previously reported in rodent models of neural degeneration. Schwann cells adopted a repair phenotype in acutely injured nerve samples which faded over time with chronic denervation. This finding may assist clinicians to optimize the timing of surgical nerve repair, to understand how pharmacological interventions might be used to improve clinical outcomes following surgery, or perhaps to ensure that surgery is not necessary.