MECP2 and Rett syndrome: Since the expression of PCDHB1 is not detectable in normal brains during development [37], the presence of PCDHB1 in the brains of RTT patients and the up-regulation of PCDHB1 in Mecp2-null mice may be associated with the neurological findings in RTT brains, such as decreased neuronal size, increased cell density and reduced dendritic arborization [5,37-39].