HYAL1 and hereditary disease: Although the loss of exoglycosidases to hydrolyze glycosaminoglycan oligosaccharides leads to severe genetic disorders, mucoplysaccharidoses [6], a patient with a deficiency of HYAL1 was reported to show a mild clinical phenotype [29], suggesting that exo-type CS/HA-degrading enzymes play the major role, and the contribution by endo-glycosidases might be small in the catabolism of CS/HA.