Compared with the control group, we found that C/EBPα-p30 significantly promoted the progression of AML, while both C/EBPα S16E and C/EBPα inhibited the progression of AML and the inhibitory effect of C/EBPα S16E was stronger than that of the WT group (Fig. 5h, i). The gene discussed is CEBPA; the disease is acute myeloid leukemia.