However, reports have shown that silencing CENPF using in vitro models abolished invasion in gastric cancer [46], resulted in the cell cycle arrest at G2/M checkpoint in hepatocellular carcinoma [47], reduced levels of epithelial-mesenchymal transition markers, inhibited cell proliferation, migration, and invasion, reduced global bio-energetic capacity and altered the global metabolic profiles in prostate cancer [43, 53]. The gene discussed is CENPF; the disease is gastric cancer.