These observations, along with dysregulation of FERMT3, ILK, TLN1 and VCL in fragile X PBMCs suggest that deregulation of integrin activity plays a role in FXS molecular physiopathology and that peripheral blood cells, such as PBMCs or platelets, are relevant models to address this hypothesis54,79,83–85. This evidence concerns the gene VCL and fragile X syndrome.