Nevertheless, as the transcriptional regulation of the mouse and human ABCC6 genes is similar (Aranyi et al., 2005; Douet et al., 2006, 2007; de Boussac et al., 2010; Ratajewski et al., 2012), it is likely that the human β-thalassemia phenotype could induce comparable molecular changes leading to a suboptimal endowment in ABCC6 and increased susceptibility to ectopic mineralization in a PXE-like manner. Here, ABCC6 is linked to pseudoxanthoma elasticum (inherited or acquired).