American Society of Hematology, Blood, 16(130), p. 1845-1856
DOI: 10.1182/blood-2017-05-786004
Full text: Unavailable
Key Points There is heterogeneity in the clinical, laboratory, and genetic bases of HX. Alterations in PIEZO1 channel kinetics, response to osmotic stress, and membrane trafficking may contribute to channel dysfunction in HX.