Anderson–Fabry disease (AFD) is a lipidosis caused by deficient αGLA (α-galactosidase A) enzyme activity due to a mutation in the galactosidase alpha gene leading to progressive lysosomal accumulation of complex sphingolipids in vascular endothelial and smooth-muscle cells throughout the body and in the cells of kidney, nervous system, eyes, and heart (1, 2). Here, GLA is linked to Nager acrofacial dysostosis.