While inhibition of noncanonical TGF‐β signaling ameliorates aortic aneurysm progression in MFS mice [43], our iPSC–SMC model showed hyperactivation of noncanonical ERK1/2 signaling and reduced Smad2 activity in response to TGF‐β in patient‐derived SMCs (Figure 5A). This evidence concerns the gene SMAD2 and aortic aneurysm.