Moreover, alteration of ongoing mechanisms that promote Tf-TfR turnover may be involved: for instance, insulin stimulated redistribution of TfR to the plasma membrane [64], hemochromatosis protein co-trafficked with the TfR to the cell surface [65] and PI3kinase-mTOR regulated the number of TfR per endocytic vesicle [66]. This evidence concerns the gene MTOR and hemochromatosis type 1.