HDAC9 and glioblastoma: Initial research on the function of KDM1A in GBM focused on the similarities in the catalytic domain between KDM1A and monoamine oxidases (MAOs), finding that inhibition of KDM1A with the MAO inhibitor tranylcypromine rendered GBM cell lines more sensitive to treatment with HDAC inhibitors, but this synergistic effect was not observed in immortalized human astrocytes (106).