In BPDCN, the high prevalence of marrow CH and the frequent sharing of TET2 mutations with associated myeloid malignancies support a model in which CH-derived ancestral clones undergo lineage-specific transformation driven by microenvironmental cues and secondary mutational events (5), consistent with the mechanism of UV-induced pDC leukemic transformation observed in the skin (7). The gene discussed is TET2; the disease is cyclic hematopoiesis.