Studies in a G6PC3‐deficient mouse model that phenotypically and biochemically mimics neutrophil 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 blood levels of 1,5‐AG‐6P and consequently restore a normal neutrophil count.9 The gene discussed is SLC5A2; the disease is glycogen storage disease Ib.