Studies have shown that Srpk1 was increased in AD and regulated the production of tau protein, which predominantly contains four microtubule-binding repeats, which resulted in frontotemporal dementia;22,23 Fkbp5 interactions with Hsp90 promoted neurotoxic tau accumulation and increased tau stability and polymerized microtubules,24,25 indicating that E230001N04Rik might regulate tau protein accumulation by Srpk1 and/or Fkbp5 in AD progression. This evidence concerns the gene FKBP5 and Alzheimer disease.