FMR1 and fragile X syndrome: In addition, FXS animal models have Fmr1 gene deletion rather than epigenetic silencing of FMR1 as a result of CGG expansion observed in a majority of human FXS patients, therefore Fmr1-KO rodent models cannot fully model the genetic complexity in human FXS including CGG expansion and retraction, DNA demethylation or loss of CGG repeats leading to FMR1 gene reactivation, and somatic mosaicism [93, 94].