SLC5A2 and glycogen storage disease Ib: Studies in a G6PC3-deficient mouse model that phenotypically and biochemically mimics the PMN impairment of patients with GSD Ib have shown that treatment with an inhibitor of the kidney sodium glucose co-transporter 2 (SGLT2) was able to lower the blood level of 1,5AG6P and consequently restore a normal neutrophil count [10].