Overexpression of Pfdn5 suppressed not only hTauV337M-induced neurotoxicity but also in a different Tauopathy model, hTauR406W, which causes more severe neurotoxicity than hTauV337M in the fly compound eye (degenerated eye area: GMR-Gal4 >UAS-hTauR406W: 82.15±3.194 vs. GMR-Gal4 >UAS-hTauR406W; UAS-Pfdn5: 63.11±3.49) (Figure 6—figure supplement 2C–E), indicating that Pfdn5 can mitigate the neurodegeneration caused by at least one another variant/structural conformation of hTau. Here, LGALS4 is linked to tauopathy.