Additional cellular abnormalities identified in this region include dysregulated levels of Bcl-2 and P53, which have been implicated in disrupted apoptotic processes in autism [37]; dysregulation of fragile X mental retardation protein and metabotropic glutamate receptor 5, which are linked to cognitive deficits and seizure disorders in ASD [38]; altered expression of cyclic adenosine monophosphate-specific phosphodiesterase-4 (PDE4) A and B proteins [39]; and increased expression of connexin 43, indicative of abnormal glial–neuronal communication [40]. Here, BCL2 is linked to epilepsy.