Consistent with our results, IL-1β increased ATF5 expression in HepG2 cells (human liver cancer cell line) in a dose-dependent manner; furthermore, knockdown of ATF5 in HepG2 cells resulted in increased IL-1β-induced expression of serum amyloid A protein 1 (SAA1) and SAA2, which are acute-phase isotypes produced in response to inflammatory stress [43]. This evidence concerns the gene SAA2 and liver cancer.