Combined with the results for 2‐h PG and Δ2‐h PG, we can presume that GCK‐MODY patients have a better glucose metabolism compared to those with HNF1A‐MODY and type 2 diabetes; they exhibit lower glucose excursion, which means their islet cells function well in antagonizing postprandial hyperglycemia. The gene discussed is HNF1A; the disease is Hyperglycemia.