BACE1 and Alzheimer disease: Facilitating G4-mediated exon splicing by knocking down hnRNPH promotes the production of a shorter alternative BACE1 isoform that decreases Aβ production, suggesting G4-mediated splicing as a potential therapeutic strategy to mitigate the production of this AD-associated peptide (Hanna et al., 2021) (Figure 3A).