The cis conformation of a pSer/pThr-Pro site is resistant to dephosphorylation by both PP2A and PP5,26 and potentially the overexpression of FKBP51 can lead to hyperphosphorylation of tau, which in turn aggregates into neurofibrillary tangles that ultimately drive the development of AD. The gene discussed is FKBP4; the disease is Alzheimer disease.