In the event of nerve injury, mitochondria dysfunction emerges as a consequence of excessive reactive species production, Exceeded by endogenous antioxidant systems, triggering mitochondrial fission and an unpaired expression of mitochondrial transcription factor A (TFAM) and mitofusin 2 (MFN2) proteins, responsible for mitochondrial biogenesis and fusion, respectively, and hence, contributing to oxidative stress and increased mitochondrial damage [101]. Here, TFAM is linked to injury.