In neuromuscular disorders such as myasthenia gravis, the reduced long-term efficacy of cholinesterase inhibitors may be linked to compensatory homeostatic plasticity triggered by altered postsynaptic potentials.221 Similarly, in conditions like amyotrophic lateral sclerosis (ALS), Lambert-Eaton myasthenic syndrome, and age-related sarcopenia, impaired NMJ plasticity contributes to progressive muscle degeneration, reduced muscle mass, and increased fatigue.222. This evidence concerns the gene BCHE and amyotrophic lateral sclerosis.