NFKB1 and neoplasm: In vitro experiments confirm that VA inhibits NF-kB activation in cancer cells. In addition, analysing gene expression data in patients taking oral valproic acid showed that this drug decreased the expression of antioxidant enzymes, culminating in increased oxidative stress in tumour cells. Analysis of publicly available genome-wide drug-induced effects reveals that valproic acid, as a histone deacetylase inhibitor (HDACI), is the most effective drug in disturbing the signalling pathways activated by tumour–stromal interaction.