Moreover, a FMRP(1–297)-tat peptide introduced to Fmr1 KO mice by tail vein injection restores Cav3–Kv4 complex function and mossy fiber LTP, reduces the level of activity in adult animals within 1 h, and rescues disrupted translation of select proteins associated with FXS for at least 24 h, supporting the potential for a tat-FMRP conjugate approach to be developed as a therapeutic agent for FXS. Here, KCNC1 is linked to fragile X syndrome.