More importantly, selective clearing of p16‐expressing cells with a genetic approach or eliminating senescent cells using senolytic compounds in AD mouse models have been shown to ameliorate various aspects of AD pathologies including tau phosphorylation, neurofibrillary tangles (NFTs) formation, Aβ load, and cognitive decline (Bussian et al. 2018; Hu et al. 2021; Musi et al. 2018; Zhang et al. 2019). This evidence concerns the gene CDKN2A and Alzheimer disease.