For example, excess of accumulated glycosaminoglycans and defective proteoglycan desulfation have been shown to alter fibroblast growth factors‐2 (FGF2)‐heparan sulfate interactions and the FGF2 signaling pathway in a murine model of MSD (Settembre et al, 2008b), and bone morphogenetic protein (BMP)‐4 signaling activity in mucopolysaccharidosis type I cells (Pan et al, 2005). This evidence concerns the gene FGF2 and Multiple sulfatase deficiency.