Research has shown that FMRP plays a critical role in the development of interneurons (INs), with its deficiency leading to a widespread downregulation of GABAergic transmission.[20, 21] Restoration of GABA receptors (GABARs) expression can modulate the excitability of pyramidal neurons (PNs) and improve cognitive behaviors in FXS mice.[22, 23] These findings underscore the pivotal role of GABAergic transmission in the pathophysiology of FXS and offer a theoretical foundation for exploring the therapeutic potential of MGE‐derived GABAergic progenitor cells in FXS treatment. Here, FMR1 is linked to fragile X syndrome.