Our team has shown that the FKBP52 interaction with Tau (both wild-type and TauP301L) has a considerable impact on the progression of the early manifestations of the tauopathy in vivo, because in the model of hTau-P301L zebrafish mutant used for the study, the early axonal growth defects are rescued by FKBP52 knock down [54]. The gene discussed is FKBP4; the disease is tauopathy.