FBN1 and type 2 diabetes mellitus: It may also explain why some Marfan patients (such as our case with an exon 25 mutation [8]) have reduced adipose regardless of dietary intake while others have normal or even excess adipose and consequent type II diabetes (for example some members of the family described in [67]), since the production of asprosin would depend on whether the furin site was able to be cleaved to produce the C-terminal fragment.