Given that excessive SMAD signaling is the common denominator in all syndromic and nonsyndromic aneurysms (Gomez et al., 2009) and that TGF‐β has a key function as driver of SMC differentiation (Guo & Chen, 2012), our findings suggest that increased SMC differentiation might be a possible underlying driver toward aneurysm development in patients with this pathogenic TGFBR1 mutation. This evidence concerns the gene TGFBR1 and aneurysm.