Mutations in founder (TET2, ASXL1 and ZRSR2) and progression (NRAS; KRAS; loss of chromosome 9 or 3p harbouring CDKN2A or SETD2, respectively) genes were all more frequent in BPDCN than CMML and/or AML, supporting privileged roles in BPDCN pathogenesis (Fig. 1f and Extended Data Fig. 1h). The gene discussed is ASXL1; the disease is CD4+/CD56+ hematodermic neoplasm.