In vivo G-CSF therapy corrects neutropenia and improves neutrophil function in G6pc3^−/− mice. G6pc3^−/− (−/−) and control (+/+) littermates were treated with recombinant mouse G-CSF for 1 or 5 days. (A) Blood and BM neutrophil counts in untreated and G-CSF–treated mice. (B) Representative flow cytometric analysis of neutrophil p-Akt, membrane-bound PtdIns(3,4,5)P₃, and active caspase-3 in 5-day G-CSF–treated control and G6pc3^−/− mice. (C) Neutrophil respiratory burst activity in response to 200 ng/mL of phorbol myristate acetate in untreated and 5-day G-CSF–treated control (○) and G6pc3^−/− (●) mice. (D) Neutrophil concentration-dependent chemotaxis in response to fMLP in untreated and 5-day G-CSF–treated control (○) and G6pc3^−/− (●) mice. (E) Neutrophil calcium flux in response to 10⁻⁶M of fMLP in untreated and 5-day G-CSF–treated control (○) and G6pc3^−/− (●) mice. Data are the mean ± SEM of 3 (untreated) or 6 (G-CSF–treated) independent experiments. *P < .05.