FMR1 and fragile X syndrome: Only human FMR1 rescues the broad range of neurological phenotypes caused by dFMR1 KO, with human FXR1/2 having no activity, showing that FMR1 function has been evolutionarily conserved and that human FMR1 requirements can be effectively dissected in the Drosophila FXS disease model [84, 99].