In agreement with this notion, the reduction in the content of MBP in the spinal cord of ALS and FTD patients with TDP43 proteinopathy did not correlate with the decrease in the number of mature oligodendrocytes, which strongly suggests that certain myelin modifications can take place, at least in part, as an independent event (Rohan et al., 2014). The gene discussed is MBP; the disease is proteostasis deficiencies.