Parone et al. (2013) demonstrated that protection of motor neuron mitochondria in the spinal cord induced by inhibiting cyclophilin D (a key regulator of calcium-mediated opening of the mitochondrial transition pore, mTP) in three varieties of superoxide dismutase 1 (SOD1) mutations, despite preserving the number of motor neurons counted in the spinal cord, did neither mitigate symptoms nor prolong survival in experimental ALS. Here, SOD1 is linked to amyotrophic lateral sclerosis.