Overall, founder clones contained recurrent alterations in TET2 (5 out of 5 cases, 4 out of 5 cases with ≥2 alterations), ASXL1 (3 out of 5 cases) and splicing-factors (3 out of 5 cases), including ZRSR2 (2 out of 5 cases), suggesting privileged roles in premalignant evolution in BPDCN (Fig. 1e (top)). This evidence concerns the gene TET2 and CD4+/CD56+ hematodermic neoplasm.