We havepresented data in support of an anti-tumour mechanism for NFκB1 viap50:p50-mediated transcriptional repression of neutrophil-recruiting chemokines.From our observations, we predict that enhancing the anti-inflammatory properties ofp50:p50 and its co-repressor HDAC1 in hepatocytes would have suppressive effects onthe hepatic expression of multiple neutrophil chemokines, thereby limiting hepaticneutrophil accumulation and reducing the incidence of genotoxic and telomeric damagein bystander hepatocytes. This evidence concerns the gene HDAC1 and neoplasm.