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. The gene discussed is SOX9; the disease is breast cancer.