FGF23 and neoplasm: The pathophysiological mechanism is that the level of fibroblast growth factor (FGF)23 secreted by the culprit tumor in the blood is increased, which inhibits the activity of 1α‐hydroxylase in the kidney and the expression of sodium/phosphorus co‐transporter, leading to increased urine phosphorus excretion and reduced absorption of phosphorus in the small intestine, resulting in hypophosphatemia.13