To date, the biopsychological implications of CaMKIIα-dependent Homer phosphorylation have been inferred from studies of the Fmr1 knock-out (KO) mouse model of Fragile X syndrome, which exhibits elevated CaMKIIα activity, Homer1 and Homer2 hyperphosphorylation and reduced Homer-mGlu5 binding (Guo et al., 2015), which can be rescued by reducing CaMKIIα activity or levels or replacement with mutant Homers that cannot be phosphorylated by CaMKIIα (Guo et al., 2015). This evidence concerns the gene CAMK2A and fragile X syndrome.