Recent studies have posited that tau acetylation at lysine 280 likely contributes to AD pathogenesis by limiting tau solubility, interfering with normal microtubule assembly mechanics, and promoting the formation of tau fibrils. In the study by Caballero et al., tau acetylation was correlated with disrupting chaperone‐mediated autophagy, thus stimulating pathological tau pathways. This evidence concerns the gene MAPT and Alzheimer disease.