In essence, failure to suppress GLS1 and PC expression may underlie the lower growth effects of selenite in p53-null H1299 than in wildtype p53 A549 cells while the different mode of PC inactivation (suppression versus inhibition) and differential suppression of GLS1 expression can contribute to the distinct action of selenite versus MSeA in lung cancer cells. The gene discussed is TP53; the disease is lung cancer.