The current definition of iron deficiency in patients with chronic heart failure (HF) is based on serum ferritin levels, which are not reliable for identifying true iron deficiency. This definition was developed to encourage the use of intravenous (IV) iron in patients with end-stage kidney disease, but it does not accurately reflect the iron status in HF patients. Iron deficiency in HF can be either absolute (depletion of total body iron stores) or functional (impaired mobilization of iron from stores). Functional iron deficiency is more common in HF patients and is characterized by low transferrin saturation (TSAT) but normal or elevated serum ferritin levels. The current definition, which uses serum ferritin levels to identify iron deficiency, includes patients who are not truly iron deficient and may not respond to IV iron therapy. The most reliable indicator of iron deficiency in HF is hypoferremia, defined by a TSAT <20%. Patients with hypoferremia show significant improvement in symptoms and functional capacity with IV iron therapy and have a reduced risk of cardiovascular death or heart failure hospitalizations. Therefore, the current ferritin-driven definition of iron deficiency in HF should be abandoned in favor of a definition based on hypoferremia (TSAT <20%). The use of IV iron in HF patients is more effective when guided by TSAT rather than serum ferritin levels. Additionally, the use of certain medications in HF patients, such as neprilysin inhibitors and sodium-glucose cotransporter 2 (SGLT2) inhibitors, can affect iron biomarkers and may lead to an apparent increase in iron deficiency. The findings from clinical trials suggest that TSAT is a better predictor of response to IV iron therapy in HF patients than serum ferritin levels. Therefore, the definition of iron deficiency in HF should be based on TSAT rather than serum ferritin levels.The current definition of iron deficiency in patients with chronic heart failure (HF) is based on serum ferritin levels, which are not reliable for identifying true iron deficiency. This definition was developed to encourage the use of intravenous (IV) iron in patients with end-stage kidney disease, but it does not accurately reflect the iron status in HF patients. Iron deficiency in HF can be either absolute (depletion of total body iron stores) or functional (impaired mobilization of iron from stores). Functional iron deficiency is more common in HF patients and is characterized by low transferrin saturation (TSAT) but normal or elevated serum ferritin levels. The current definition, which uses serum ferritin levels to identify iron deficiency, includes patients who are not truly iron deficient and may not respond to IV iron therapy. The most reliable indicator of iron deficiency in HF is hypoferremia, defined by a TSAT <20%. Patients with hypoferremia show significant improvement in symptoms and functional capacity with IV iron therapy and have a reduced risk of cardiovascular death or heart failure hospitalizations. Therefore, the current ferritin-driven definition of iron deficiency in HF should be abandoned in favor of a definition based on hypoferremia (TSAT <20%). The use of IV iron in HF patients is more effective when guided by TSAT rather than serum ferritin levels. Additionally, the use of certain medications in HF patients, such as neprilysin inhibitors and sodium-glucose cotransporter 2 (SGLT2) inhibitors, can affect iron biomarkers and may lead to an apparent increase in iron deficiency. The findings from clinical trials suggest that TSAT is a better predictor of response to IV iron therapy in HF patients than serum ferritin levels. Therefore, the definition of iron deficiency in HF should be based on TSAT rather than serum ferritin levels.