IDH mutation analysis is not suitable for the routine molecular diagnostic algorithm in myeloproliferative and myelodysplastic neoplasms.

tion may represent a pathophysiologically important T-cell subpopulation involved in the characteristic progressive loss of hematopoietic stem cells from the bone marrow microenvironment in AA. Related, others have previously shown that T lymphocytes are a potent source of inflammatory and regulatory cytokines, including interleukin 10 (IL-10), reported to be elevated in a subgroup of patients with severe AA and more recently in patients with ALPS.3,7 Alternatively, abnormal T-cell biogenesis is merely an epiphenomenon in AA, and perhaps in ALPS, that indicates a common pathway of dysregulation leading to autoimmunity. In conclusion, our retrospective analysis for the first time demonstrates the existence of a sizable population of doublenegative T cells in AA patients, suggesting that DNTs represent a sensitive but not necessarily specific marker of ALPS. Further investigation may demonstrate previously unrecognized overlap in pathogenesis of AA and other immune cytopenias. Clearly, our observation of peripheral expansion of TCR–expressing DNT cells in AA warrants the prospective study of a larger cohort and may lead to additional diagnostic and therapeutic approaches.