Overexpression of SELENOS attenuated the reduction in RAW264.7 macrophage viability and the increase in cell apoptosis induced by TG and TC [21], inhibition of SELENOS expression in mouse astrocytes further aggravated the reduction in cell viability induced by TG and TC [60], and inhibition of SELENOS expression in HepG2 liver cancer cells further aggravated cell apoptosis and further reduced the cell viability induced by β-mercaptoethanol [61]. Here, SELENOS is linked to liver cancer.