Following on from this observation, we hypothesized that preventing the Hsp90-dependent action of FKBP51 with LA1011 could perhaps reduce the phosphatase-resistant cis conformation of pSer/pThr-Pro bonds at multiple tau sites, and in turn limit or prevent the hyperphosphorylation of tau and the development of AD. The gene discussed is FKBP4; the disease is Alzheimer disease.