This is in line with previous papers showing a differential pyramidal tract degeneration in homozygous SOD-1D90A ALS and sALS [47–49]; e.g., Blain and colleagues have recently reported a marked reduction in fractional anisotropy in the corticospinal tract in patients with sALS and fALS, despite similar levels of upper motor neurons dysfunction and overall clinical disability [47]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.