Indeed, we found no evidence that ASO‐21 treatment altered Aβ abundance in AD mice, suggesting that the improvement in synaptic function associated with the increase in exon 19 splicing is not mediated by a direct reduction in Aβ, per se, but rather may result from increased competitiveness of the exon 19‐containing ApoER2 isoform for Reelin and consequently the improved likelihood of forming a functional ApoER2/Reelin signaling complex. The gene discussed is RELN; the disease is Alzheimer disease.