Indeed, over-activation of SFKs in cancer cells has been found to be a result of one of the following contributing events: (i) upregulation of the phosphatases that target the inhibitory C-terminal tail phosphotyrosine [16, 17], (ii) reduced expression of Chk [18] and (iii) reduced expression of the scaffolding protein Cbp/PAG1 that directs co-localization of Csk and Chk with SFKs [19, 20]. The gene discussed is CSK; the disease is cancer.