Specifically, these overlapped genes included C/EBPβ and JMJD3 themselves, other myelopoietic regulators and innate immunity components such as JUNB, IER3, CCNG2, SPRY4, ICAM1, P53-P21 axis, IL-1β, and S100A9 (but not RIPK3) (Fig. 6b, d, e and Supplementary Fig. 6a, b), thus indicating C/EBPβ as one of the principle TFs that recruited JMJD3 to the target promoters and the existence of a positive feedback mechanism of JMJD3 regulatory effect through activating C/EBPβ expression in AML cells. The gene discussed is TP53; the disease is acute myeloid leukemia.