TAFAZZIN and Fabry disease: In addition, the majority of the FD phenotype was originally thought to be driven directly by the increase in cAMP after activation of the Gs pathway,80 but data published over the past several years have suggested that ancillary pathways activated by Gsα, such as Wnt,18 Hedgehog,18,30 and Yap/Taz,31 are major contributors to the abnormal bone formation in FD.