In mice overexpressing CDT2, degradation of p21 released CDKs' activity toward cell cycle progression and triggered AD processes, including increases in amyloid‐beta, p‐tau, and BACE; memory deficits; and a gene expression signature similar to that observed in human AD, for example, increases in APOE, CASS4, and CLU. This evidence concerns the gene CASS4 and Alzheimer disease.