Transferrin structure, metabolism and physiological functions (iron transport, activation of cellular growth, bacteriostatic effect) are described with reference to the last informations available from the literature. This analysis results in a better understanding of the mechanisms involved in its physiopathological variations. Decreased serum transferrin levels are the result of a reduction of the biosynthesis (hepatic deficiencies, malnutrition), or an increase of catabolism (acute, chronic and malignant infections), or an increase of intestinal or renal losses, or very infrequently genetic disorders. Increased serum transferrin levels are the result of either hyposiderosis or an oestrogenic impregnation. Alcoholism and diabetes are responsible of qualitative modifications of this protein.