The central hypothesis investigated in this study was that treatment with a CRISPR-based RNase targeted to an antisense RNA will allow increased expression of the key therapeutic gene, UBE3A, in human cells and and mouse models of Angelman syndrome. All hypotheses are falsifiable, and in fact the experimental data indicated that the CRISPR-based RNases used in this study were not able to increase expression of UBE3A. It is possible that these unexpected results are due to unappreciated aspects of these proteins that make them unsuitable for this task. Alternatively, it could be that the conditions necessary for success were not achieved during the duration of the the experiments. Further work would be required to distinguish these possibilities.