In a study that included 1009 probands with pathogenic FBN1 mutations (320 under 18 years of age), Faivre et al. [68] shows that nonsense, frameshift, and splicing mutations in exons 24–32 were detected only in 27.8% of patients compared to all other exons (44.4%), and nonsense mutations were not present in any patients with neonatal MS [68]. This evidence concerns the gene FBN1 and myeloid sarcoma.