This in turn would hamper HDAC1‐mediated deacetylation of C/EBPβ, leading to an increase in NAG‐1 expression, and subsequently amelioration in HCC. Notably, cotreated OA (50 μM) significantly induced NAG‐1 expression in the cytoplasm and nucleus of HCC cells, increasing the acetylation of the C/EBPβ transcription factor, while decreasing HDAC1 protein. The gene discussed is GDF15; the disease is hepatocellular carcinoma.