Hypomagnesemia has been shown to diminish tyrosine kinase activity at the insulin receptor level, resulting in decreased insulin-receptor interactions.[22,28,29] Additionally, RAAS activation may lead to insulin resistance.[30] Despite these insights, the precise mechanism of abnormal glucose metabolism and insulin secretion in GS patients remains elusive and warrants further exploration in clinical trials. This evidence concerns the gene INS and familial primary hypomagnesemia.