The EC50 in HeLa cells for panobinostat was 0.1 μM. Against cervical cancer cells, this drug was able to reduce the cell viability in a dose- and time-dependent manner. Panobinostat increased reactive oxygen species levels inside the cells, disrupted mitochondrial membrane potential, increased levels of p21 and caspase-9, and reduced the expression of Bcl-xL genes. This evidence concerns the gene CASP9 and cervical cancer.