Finally, with regard to how MYORG contributes to PFBC, the ER localization of MYORG, coupled with its now established glycosidase activity and similarity to ER α-Glu II, makes it tempting to suggest that dysfunction of MYORG as seen in PFBC, may arise because of a role in quality control where it may regulate the folding or maturation of one or more of the protein products of genes linked to PFBC including SLC20A2, PDGFB, PDGFRB, and XPR1 [2–5]. This evidence concerns the gene SLC20A2 and bilateral striopallidodentate calcinosis.