Pharmacologic data on aspirin indicate that systemic concentrations of aspirin, reached with low doses (75-325 mg once daily), are inadequate to permanently acetylate COX-2 but are optimal for its metastatic chemoprevention through inhibition of platelet activation and thrombocytosis [38], inhibition of MMP-2 activity and increase in E-cadherin production [39], down-regulation of an epithelial-mesenchymal-like phenotype [40], and inhibition of platelet-mediated nuclear factor-kB signaling in CTCs. The gene discussed is CDH1; the disease is thrombocytosis disease.