GAP-43 was shown to promote neurite outgrowth during development and nervous system repair by inducing F-actin accumulation, stimulating morphogenic activity, and preventing growth cone retraction (Zhang et al., 2018; Camporesi et al., 2020); changes in GAP-43 expression have been reported following nerve injury and in CNS diseases such as stroke, Alzheimer disease, epilepsy, and Parkinson disease (Tönges et al., 2014; Nemes et al., 2017; Sandelius et al., 2018; Sandelius et al., 2019; Tible et al., 2020). Here, GAP43 is linked to injury.