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. The gene discussed is INSR; the disease is familial primary hypomagnesemia.