Literature review indicated that 14% to 60% of GS patients may have abnormal glucose metabolism,[21] and the prevalence of diabetes is higher in GS patients compared to the general adult population.[21–23] The primary contributors to diabetes in GS patients are considered to be hypokalemia and hypomagnesemia.[22] Hypokalemia hampers the closure of ATP-sensitive potassium channels and L-type calcium channels on β-cell surfaces, impeding glucose-stimulated insulin secretion.[24–27] Magnesium plays a pivotal role in over 300 enzymatic reactions, particularly phosphorylation. Here, INS is linked to familial primary hypomagnesemia.