GLA and Fabry disease: Furthermore, neutralizing ADA had inhibitory function via directly binding agalasidase beta or modulating its signaling pathway, which probably led to adverse impacts on the PK and efficacy.[29] Previous studies demonstrated that the types and doses of ERT (e.g., agalsidase alfa and agalsidase beta) had different risks and effects on developing ADA in FD.[30] The clinical significance of ADA in FD is still under research.