As an example, NRBF2 (nuclear receptor‐binding factor 2; a component of the PtdIns3K complex I) interacts with APP and favors its lysosomal disposal, as demonstrated by the fact that NRBF2 depletion leads to excessive levels of intracellular APP in cells (Yang et al, 2017b) and Aβ accumulation in AD mouse models (Lachance et al, 2019), whereas overexpression of NRBF2 reduces Aβ levels and improves mouse memory (Lachance et al, 2019). This evidence concerns the gene APP and Alzheimer disease.