Since it has been known for decades that the so-called premutation range (55-200) CGG repeats on the FMR1 (fragile X) gene predispose towards premature ovarian failure (POF) [1], it is actually remarkable that, until relatively recently, nobody had explored the gene in terms of its relationship to ovarian function. This is even more notable since, in 1991, Fu et al. reported a significant distribution peak of 29-30 repeats in the general population, with relatively minor 'noise' at lower and higher counts (Figure 1) [2].This distribution peak has no apparent relevance to the known physiologic functions or to neuropsychiatric risks, which are the principal reason as to why CGG counts on the FMR1 gene are currently clinically evaluated [1]. More importantly, current definitions of what represents normal counts or ranges that denote risk (common or normal: <40/45; intermediate or gray-zone: 40/45-55; premutation: 56-200; full mutation: >200), are practically exclusively determined by the risk for neuropsychiatric conditions [1]. Therefore, the reason that nobody has yet explored a possible separate function for Fu's distribution peak of 29-30 CGG repeats is somewhat puzzling.
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