Our results showed that silibinin treatment led to the cleavage of caspase 3 and PARP-1 in both SR and A172 cells in a concentration-dependent manner (Figure 2(b)), indicating that silibinin induces glioblastoma cell apoptosis via a caspase-dependent PARP-1 cleavage, which has been widely considered to be a hallmark of apoptosis. The gene discussed is CASP3; the disease is glioblastoma.