To explore the mechanisms underlying platelets mediated colon cancer cells’ proliferation, we examined if any alteration of cell cycle occurred, by analyzing the regulators of cell cycle progression (CyclinD1, CyclinE1 (Ccne1) and proliferating cell nuclear antigen (Pcna) and the tumor suppressor Pten (phosphatase and tensin homolog deleted on chromosome ten), which is frequently modified in human cancers, including breast, lung, prostate and bladder cancer [18]. The gene discussed is PTEN; the disease is cancer.