Remarkably, for the first time, we demonstrate that the efficacy of bLf in treating anemia and AI in β-thalassemic and HT women, respectively, can be correlated, in addition to the decrease to the IL-6, with two potential different molecular mechanisms: hepcidin-independent for β-thalassemic and hepcidin-dependent for HT women. The gene discussed is HAMP; the disease is hematocrit.