Studies on cancers, such as lymphoma [31, 32], prostate cancer [33], neuroblastoma [34], and other malignancies [35], demonstrate that CDK9-related pathways are dysregulated, suggesting that CDK9 overexpression promotes the cell proliferation and the synthesis of antiapoptotic factors like MCL-1, BCL,-2 and XIAP [36], which are determinants for cancer-cell survival [37]. This evidence concerns the gene CDK9 and prostate carcinoma.