It was shown that Smad2 promoter activation is driven by the recruitment of a multipartner complex, including the transcription factor p53 and histone acetyltransferases.48Remarkably, the transcriptional regulatory network of the Smad2 promoter was dramatically altered in human aneurysmal aSMCs in vitro and in situ with a switch from Myc-dependent repression of Smad2 in normal vessel to a p53-dependent constitutive activation of Smad2 in aneurysms. The gene discussed is TP53; the disease is aneurysm.