In GTEx [15], this variant is an eQTL strongly associated with decreased expression in whole blood (p = 1.7x10-37), which would be concordant with the known molecular mechanism of FBN1 pathogenesis in MS: pathogenic alleles impairing gene function result in increased height and abnormal fat distribution and increased arterial stiffness [16, 17]. Here, FBN1 is linked to myeloid sarcoma.