If there was a high expression of acetylcholine receptors you would expect a high peak response and no prolonged response. The Vance Spence's group found a normal peak response and a prolonged response in the CFS patients which is consistent with low cholinesterase levels.
That would be true if the gene expression of cholinesterase were the same in the normals and the PWCs, but suppose the expression of cholinesterase drops in PWCs, as another adaptation to lower acetylcholine production in addition to a rise in expression of the acetylcholine receptors, both due in turn to choline deficiency resulting from the methylation deficit? I think this would be likely, if acetylcholine is indeed low in PWCs. I think all this fits together well. I would like to see some good measurements of absolute choline and acetylcholine levels. I don't know why the pyridostigmine seemed to help some PWCs, while the galantamine did not.