Moreover, we suggest that this would lead to cellular stress of Tns3-deleted differentiating oligodendroglia and to the upregulation of p53, master regulator of cellular stress and apoptosis, which has been previously been shown to be involved in the apoptosis of human OLs in the context of MS (Ladiwala et al., 1999; Wosik et al., 2003) and in the cuprizone demyelination mouse model (Li et al., 2008; Luo et al., 2021). Here, TNS3 is linked to myeloid sarcoma.