In early studies, Byrne pointed out that in patients with GCK-MODY, the glucose sensitivity of pancreatic β-cells was reduced, and the threshold for insulin secretion was increased due to the decrease in GCK activity induced by heterozygous mutations in the GCK gene; thus, patients with GCK-MODY showed a higher level of FBG compared to the controls (Byrne et al., 1994). The gene discussed is GCK; the disease is MODY.