Given the positive correlation between the expression levels of p53 and CBFB in a variety of AML cases as shown in Fig. 1b, it is likely that RUNX1 depletion-mediated up-regulation of CBFB is under the control of the accumulated p53, and thus creating an autonomous RUNX1-p53-CBFB feedback loop regulatory system for AML cell proliferation (Fig. 1g). The gene discussed is TP53; the disease is acute myeloid leukemia.