Importantly, the human diseases (Fanconi anemia, BS, and WS) resulting from deficiency of FANCJ, BLM, and WRN, respectively, all exhibit genomic instability that may be related, in part, to inability to resolve G-quadruplex structures [50] and deficiencies in Sgs1, WRN, and BLM have been linked to alterations in gene expression related to potential G quadruplex-forming sequences in transcriptional units [34], [51]. This evidence concerns the gene WRN and Werner syndrome.