Considering that the anti-tumor potency of RUNX gene silencing is highly dependent on functional p53 with the sequence-specific transactivation capability, we have sought to examine a possible involvement of p53 in the transcriptional regulation of CBFB. Close inspection of the gene expression profiles in de novo AML patients from two independent studies revealed the presence of the positive correlation between the expression levels of p53 and CBFB (Fig. 1b). The gene discussed is CBFB; the disease is neoplasm.