As AD had been shown previously to be caused by mutations in ADAMTSL2 [25] and a direct interaction between FBN1 and ADAMTSL2 was found, the authors suggested that a dysregulation of the FBN1/ADAMTSL2/TGFβ interrelationship lay at the basis of the AD/GD phenotypes. Here, TGFB1 is linked to Alzheimer disease.