FMR1 and fragile X syndrome: In accordance with these findings, increased mGluR5-signaling-dependent AMPAR endocytosis or altered mGluR5–Homer scaffolds are observed in OCD models with Sapap3-mutant mice, fragile X syndrome models with Fmr1-KO mice, and autism models with Shank3-mutant mice, which all include repetitive behaviors, among other symptoms [95,101,124,125], suggesting a potential shared genetic mechanism of different neuropsychiatric disorders (Figure 2).