[1] Early research into the disorder was conducted by a team led by Anthony S. Pagliara and Barbara Illingworth Brown at Washington University Medical Center, based on the case of an infant girl from Oak Ridge, Missouri.

This is the time when liver glycogen stores have been exhausted, and the body has to rely on GNG.

When given a dose of glucagon (which would normally increase blood glucose) nothing will happen, as stores are depleted and GNG doesn't work.

[4] To treat people with a deficiency of this enzyme, they must avoid needing gluconeogenesis to make glucose.

As with all single-gene metabolic disorders, there is always hope for genetic therapy, inserting a healthy copy of the gene into existing liver cells.