I'm thinking Acetylcholinesterase affects the Neuromuscular junction (NMJ). Acetylcholinesterase breaks down Acetylcholine after it has stimulated the post-synaptic receptors. Thus, the enzyme stops the activation of the muscle.
Some toxins work on acetylcholinesterase by degrading it, which results in constant tetanus becuase acetylcholine will be left in the synaptic cleft and will keep stimulating the post-synaptic receptors, resulting in paralysis, and loss of vital processes like breathing.