Changes in the equilibrium of the antagonistic kinase and phosphatase activities, especially on tyrosine residues, have been described in many cancers as a result of the oncogenic activation of receptor or non-receptor tyrosine kinases or the inhibition of protein tyrosine phosphatases (e.g., EGFR, Her-2neu, Src, Abl, PTPs) [28]. This evidence concerns the gene PTS and cancer.