Previous reports have suggested that motor neurons are vulnerable in ALS because they are larger than other cells; require large amounts of energy to maintain homeostatic ionic gradients and generate action potentials; are easily overloaded [36]; and have a lower buffering capacity for glutamate-triggered calcium ion influx [37], decreased expression of calcium-binding proteins such as CalbindinD28K and parvalbumin [38, 39], and decreased expression of GABAA receptor α1, which is involved in inhibitory synaptic transmission [40, 41]. The gene discussed is PVALB; the disease is amyotrophic lateral sclerosis.