With regard to the hypocalcemia, multiple factors might be involved: malabsorption of calcium from the bowel, PTH dysfunction due to hypomagnesemia, inhibition of vitamin D, and degradation of 1,25(OH)2D production due to PTH insufficiency, and elevation of FGF23.[8] It has been demonstrated that the activity of adenylate cyclase is inhibited, as well as renal and skeletal resistance to PTH action is increased under in the hypomagnesemic state.[14] In this case, serum 25-hydroxyvitamin D (25(OH)D) was undetectable in spite of vitamin D supplement. Here, ADCY1 is linked to familial primary hypomagnesemia.