Because aging‐dependent sensorimotor defects (primarily in aging males) and Purkinje cell degeneration detected in p17/PERMIT−/− mice were like those seen in patients with ALS, we measured ACO2, CerS1, and p17/PERMIT in mitochondria isolated from the verified brain tissues of patients with ALS versus non‐ALS donors (Tables 1 and 2). This evidence concerns the gene CERS1 and amyotrophic lateral sclerosis.