|Polo-like kinase 1 (Plk1) is a serine-threonine protein kinase that functions as a key regulator of mitosis/meiosis and cytokinesis (Barr et al., 2004). Numerous research studies have demonstrated that Plk1 gene expression is frequently up-regulated in human cancers and carcinoma-derived cell lines (Simizu and Osada, 2000). Plk1 expression levels are abnormal in many spontaneous human cancers including pancreatic, ovarian, breast, non-small cell lung carcinoma, prostate, melanoma, colorectal, and gliomas (Weichert et al., 2004; Weichert et al., 2005; Takai et al., 2005). Interest in Plk1 is based on evidence that Plk1 inhibition by Plk1-specific anti-sense oligonucleotides, siRNA, or short hairpin RNA results in decreased tumor-derived cell survival and inhibited tumor growth in animal models (Spankuch-Schmitt et al., 2002; Spankuch et al., 2004; Guan et al., 2005). These data suggest that Plk1 is a rational and validated anticancer drug target. Interestingly, there is evidence that Plk1 is a molecular target for other diseases and/or viral infections. For example, it has been shown that Plk1 protein is (1) along with other cell cycle proteins, detectable in Alzheimer’s, but not in control neurons (Harris et al., 2000; Husseman et al., 2001); (2) up-regulated in CD4+ T cells from rhesus macaques infected with high viral load SIV (Bostik et al., 2004); (3) up-regulated in primary human kertinocytes infected with human papilloma virus type 16 E6 and E7 (Patel et al., 2004); and (4) is specifically associated with and/or phosphorylates the human cytomegalovirus pp65 lower matrix protein upon infection of human fibroblasts and HeLa cells (Gallina et al., 1999). While the significance of these latter findings is undefined, it suggests that aberrant Plk1 expression may result in unregulated cell cycle events leading to cell degeneration or that pathogenic viruses express and/or recruit Plk1 for their own benefit.