Inhibiting PR70 in cancer cells with evidence of mitotic catastrophe or excessive chromosomal instability may be an attractive therapeutic approach as the depletion of PR70 induced cell death in breast, pancreatic, ovarian, glioblastoma, and prostate cancer cells harboring increased polo-like kinase 1 (PLK1) expression (136, 137). The gene discussed is PLK1; the disease is prostate carcinoma.