Since an +49A to G transition in exon 1 of CTLA-4 gene results in an amino acid substitution in the leader peptide and could influence the CTLA-4 expression in T cells, Dinčić et al. have analyzed both the separate and combined effect of IL-1β TaqI, IL-1ra VNTR, and CTLA-4 +49 A/G polymorphisms on MS susceptibility, its clinical course, and its progression in a Serbian population [123]. This evidence concerns the gene CTLA4 and myeloid sarcoma.