Despite being the less potent pan-HDAC inhibitors in our study, the use of TSA and vorinostat in murine cervical cancer cells and glioma cells, respectively, resulted in an increased expression of MHC class I and multiple components of the antigen presenting machinery in surviving tumour cells, including transporter associated with antigen processing 1 (TAP1), TAP2, low-molecular-mass protein 2 (LMP-2), and LMP-7. The gene discussed is HDAC9; the disease is cervical carcinoma.