The penetrance of FBN1 pathogenic variants is reported to be 100% [21, 22], and c.365G > A has been observed in patient with nonsyndromic TAAD [23]; however, currently, there are not enough data to determine the impact of c.365G > A variant on FBN1 protein function and TAAD pathogenesis, which includes MFS. Here, FBN1 is linked to Marfan syndrome.