In this work, the authors showed that tamoxifen-inducible, SMC-specific deletion of Tsc1 in mice, generating chronic mTOR hyperactivity in SMCs, led to the development of aneurysms in the ascending aorta characterized by typical TSC pathologic features such as aortic wall thickening, SMC proliferation, and loss of elastin fibers, a vascular phenotype that could be rescued by treating the mice with rapamycin. The gene discussed is MTOR; the disease is tuberous sclerosis.