It is still unclear how CaMKIIα perturb mGluR5 activity in FXS, however one proposed mechanism suggests that CaMKIIα is significantly elevated in the synapse of FXS mouse models, which might cause the hyperphosphorylation of the Homer 1 (H1) and 2 (H2) scaffolding proteins, resulting in their dissociation from mGluR5. The gene discussed is HOMER1; the disease is fragile X syndrome.