It has been reported that a form of AChE (a monomer lacking the peptide) is disproportionately dominant over the usual tetramer (containing the peptide) in development and that this situation is recapitulated in AD [37]: the most obvious explanation for this finding is that in both development and again in AD, the C-terminal peptide has been cleaved to operate as a signalling molecule in its own right. This evidence concerns the gene ACHE and Alzheimer disease.