As we have established that the PXE-like mineralization in β-thalassemia patients arises independently of ABCC6 mutations (Hamlin et al., 2003), we hypothesized that the expression of the ABCC6 gene or the biological properties of its product could be disrupted in liver and/or kidneys as a secondary consequence of the hemoglobinopathy. The gene discussed is ABCC6; the disease is hemoglobinopathy.