In summary, although there is no clear research evidence, the above studies have sufficiently demonstrated that the possibility of IL-23 being involved in activating PI3K/Akt and NF-κB signaling pathways is very high, and if it is clear that IL-23 can activate PI3K/Akt and NF-κB signaling pathways and be involved in the regulation of AD, it will provide new ideas for future targeted therapies. This evidence concerns the gene AKT1 and Alzheimer disease.