Since MYC and RUNX2 promote the formation of BPDCN due to the RUNX2 super-enhancer in vitro, we examined whether the over-expression of MYC and RUNX2 was sufficient for the initiation of BPDCN in the absence of Tet2 and Tp53, because loss-of-function mutations in TET2 and TP53 are the most frequently detected in patients with BPDCN regardless the presence of t(6;8)4. This evidence concerns the gene TP53 and CD4+/CD56+ hematodermic neoplasm.