In β-thal erythroblasts, mitapivat normalizes the stress-induced upregulation and nuclear recruitment of Prx-2. (A) PRDX2 gene expression normalized on HBA1 expression in CD34⁺-derived erythroid precursors, on days 7 (upper) and 14 (lower) of culture, from patients with β-thal (cod β039) in vitro treated with vehicle or mitapivat (2 μM). Data are mean ± SEM (n = 5); ^ˆP < .05 (compared with vehicle-treated cells). (B) Western blot analysis of Prdx2 in erythroid precursors, as in panel A. Catalase served as loading controls. One representative immunoblot of other 4 with similar results. (C) Prdx2 immunostaining of CD34⁺-derived erythroid precursors from HC and patients with β-thal (cod β039) in vitro treated with vehicle or mitapivat (2 μM). DAPI (4′,6-diamidino-2-phenylindole) was used to stain nuclei. Prx2 mean fluorescence in the nucleus and cytoplasm was measured using ImageJ. Four different squares and at least 150 cells were analyzed. Data are presented as median and minimum/maximum, with boxes indicating 25th to 75th percentiles; ∗P < .05 (compared with HC); ^ˆP < .05 (compared with vehicle-treated cells).