Adenosine-to-Inosine RNA editing, catalyzed by Adenine Deaminases Acting on RNA (ADAR) enzymes, challenges the central dogma of molecular biology and plays a pivotal role in brain function. Fragile X syndrome (FXS), the most common neurodevelopmental disorder causing mental retardation, arises from the loss of Fragile X Mental Retardation Protein (FMRP). Both adar and fmr1 genes are evolutionarily conserved and encode RNA-binding proteins prominently expressed in the brain, significantly contributing to the increased transcriptional complexity within the central nervous system. Evidence from previous studies in suggests that FMRP may interact with ADAR and postmortem brain analysis of patients with FXS has revealed a global bias toward hypo-RNA editing. However, the precise molecular mechanism through which FMRP regulates ADAR-mediated RNA editing remains to be determined. Cephalopods are renowned for their extensive ADAR-mediated RNA recoding, a distinctive form of transcriptome plasticity that sets it apart from conventional genome evolution. I plan to utilize cephalopods as a model to explore the potential ortholog of Fragile X protein in squid and elucidate its regulatory function on ADAR-mediated RNA editing.