To determine whether this change is caused by G-CSF therapy or a cell-intrinsic effect of tafazzin deficiency, we analyzed calcium levels in HSPC-derived neutrophils and observed an almost threefold increase in X-Rhod-1 signal in patient stem cell-derived neutrophils, compared to HC (HC = 2570 ± 671 vs. BTHS = 5662 ± 1160; P = 0.0162) (Fig. 5B). This evidence concerns the gene TAFAZZIN and hyperinsulinemic hypoglycemia, familial, 4.