Although the authors used CRISPR editing to treat FXS-like phenotypes in mice, they did so by inducing a loss of function mutation in a second gene rather than correct the initial null mutation in Fmr1; the authors suggest that while clinical trials that used drugs to reduce mGluR5 activity were disappointing, using CRISPR to target the overactivation may be more effective. Here, FMR1 is linked to fragile X syndrome.