While panobinostat revealed some cleavage of initiator caspase-9, effector caspase 3 and PARP (substrate of activated caspase 3), the combination treatment enhanced this further in U87, T98G and U251 GBM cells, in keeping with the results of the flow cytometry based cell death assays (Figure 2D and Figure S4C,D). The gene discussed is CASP3; the disease is glioblastoma.