At the molecular level, DCA induced post-transcriptional modifications of p53 with activation of the p53 transcriptional activity, as documented by the induction of canonical p53 target genes, such as MDM2, p21 and PUMA but not of BAX. Another major finding of our study was the ability of DCA to potently synergize with Nutlin-3, a non-genotoxic activator of the p53 pathway, in promoting cytotoxicity in B leukemic cell lines as well as in primary B-CLL patient cells, with significantly less toxicity on normal PBMC. The gene discussed is BBC3; the disease is B-cell chronic lymphocytic leukemia.