Interestingly, we found that AdoMet induced cell cycle arrest in GBM cells and that AdoMet treatment resulted in the increase in phosho-cdc25c protein, suggesting that AdoMet could retard GBM cell proliferation via phospho-cdc25c upregulation to arrest cell cycle progression at the G2/M phase. The gene discussed is CDC25C; the disease is glioblastoma.