c-Jun was shown to be required to prevent loss of sensory axons in a mouse model of CMT1A (Hantke et al., 2014), while mTORC1 is crucial to trigger a metabolic shift in SCs that supports axonal integrity in the context of acute and subacute nerve injury (Babetto et al., 2020). This evidence concerns the gene JUN and Charcot-Marie-Tooth disease type 1A.