FBN1 and Marfan syndrome: Another indication of the potential importance of altered protease activity for the pathogenesis of MFS is the observation that treatment of mice with mutations in the Fbn1 gene with doxycycline, a non-specific MMP inhibitor, significantly delays aneurysm rupture in MFS-like mice by inhibiting expression of tissue MMP-2 and MMP-9 and thus, degradation of the elastic matrix [32], [33].