Based on these two studies and the expression pattern of the two molecules a model was proposed for the inappropriate erythroid regulation of hepcidin in thalassaemia, where TWSG1 (produced in the early erythroblasts) acts indirectly by inhibiting the BMP–SMAD pathway and GDF15 which is produced in late erythroblasts acts directly to inhibit hepcidin, although the signalling mechanism is unknown [77]. The gene discussed is HAMP; the disease is thalassemia.