In breast cancer tissues and cells, HDAC8 expression is up‐regulated, and HDAC8 interacts with AKT1, deacetylating it at lysine 426 and activating AKT1, thereby increasing GSK‐3β phosphorylation and promoting its degradation, which triggers the spread and EMT of breast cancer cells.51 This evidence concerns the gene HDAC8 and breast carcinoma.