We focused our initial efforts on examining the role of PLK1 for several reasons: first, PLK1 functions in activating the major kinases, phosphatases and cyclins that promote mitotic entry and progression through the G2-M cell cycle check point, [29] second, PLK1 overexpression has been well documented in cells with high mitotic index including an SMC tumor, leiomyosarcoma [15], third, a number of small ATP-competitive inhibitors such as BI 2536 and BI 6727, highly selective for PLK 1, are currently in different phases of clinical trial against other common human cancers [30, 31]. Here, PLK1 is linked to cancer.