Based on the essential function of TRAF4 on TJs and published data in the field of myelin alteration, we propose the following cascade of events to explain the TRAF4-KO ataxia phenotype : the absence of TRAF4 first affects myelin TJs leading to the loss of myelin integrity, and subsequently to MAG and NogoA overexpression, activation of the NgR/p75NTR/RhoA signaling pathway, actin cytoskeleton changes, Purkinje cell death and, hence, ataxia. The gene discussed is NGFR; the disease is Ataxia.