Recently, several synaptic CAMs, such as intercellular adhesion molecule 5 (ICAM5) (Pei et al., 2020), neuroligin-1 (Dahlhaus and El-Husseini, 2010; Lai et al., 2016), N-cadherin (La Fata et al., 2014), L1-CAM (Djabali et al., 1990), and calsyntenin 1 (CLSTN1) (Cheng et al., 2019), have been found to aberrantly intervene in the pathological phenotype of fragile X syndrome (FXS), providing insights into the pathogenic mechanisms underlying FXS. This evidence concerns the gene NLGN1 and fragile X syndrome.