Of note, it has been shown that ER expression can be re-established in breast cancer cells through treatment with HDAC inhibitors [23], and we demonstrate in this study that IL-13Rα2 expression is similarly regulated in that the inhibition of either histone deacetylation or DNA methylation produced an upregulation of IL-13Rα2 expression, enhancing consequent susceptibility to Pep-1-Phor21 treatment. Here, HDAC9 is linked to breast cancer.