While the data on copy number variations seem to be rather specific for BPDCN among hematologic neoplasms, recent work [18, 29] demonstrated point mutations in TET2 und TP53 in the genome of BPDCN thereby genetically relating BPDCN to a broad range of myeloid malignancies, where recurrent mutations particularly in the tumour suppressor TET2 but also in TP53 are highly prevalent [30, 31]. This evidence concerns the gene TP53 and hematopoietic and lymphoid system neoplasm.