Higher levels of OT in WS has been hypothesized to result from the hypomethylation (and thus overexpression) of OXTR, the gene encoding the oxytocin receptor (Haas and Reiss, 2012), perhaps as a result of the hemideletion of WBSCR22, which encodes a methyltransferase (Doll and Grzeschik, 2001; Merla et al., 2002), and/or some effect of GTF2I, also deleted in WS, a gene that has been proven to affect the reactivity to OT and ultimately, sociability (Procyshyn et al., 2017). The gene discussed is BUD23; the disease is Werner syndrome.