By analyzing the CD52 expression of the TCGA cohort (Fig. 6F), we found that AML patients with del(7), inv(16), RUNX1 and DNMT3A mutations showed significantly higher CD52 expression, implying that the patients harbored these genetic alterations may be suitable for the treatment of CD52 targeted antibody alemtuzumab. The gene discussed is RUNX1; the disease is acute myeloid leukemia.