Using co-immunoprecipitation and immunoblotting of HDAC5 and SOX9, treatment with the HDAC4 and HDAC5 inhibitor LMK-235, differential gene expression analysis, HDAC5 knockouts generated using CRISPR/Cas9, and HDAC5 overexpression using plasmid transfection, Xue et al. [86] demonstrated that HDAC5 was essential for deacetylation and nuclear localization of SOX9, which was important for resistance to tamoxifen in breast cancer cell lines. Here, SOX9 is linked to breast carcinoma.