HDAC9 and breast carcinoma: Given the reliance of breast cancer cells on histone deacetylation mediated epigenetic regulation, the response to HDAC inhibitors (belinostat, HDAC- 42, panobinostat, pracinostat, ricolinostat, romidepsin, vorinostat) was similar between CTR and TIS cells, as was the response to the PI3K inhibitor duvelisib and the proteasome inhibitors bortezomib and ixazomib.