It has been shown that site-specific phosphorylation of tau at threonine 205 (T205) by the kinase p38γ disengages tau from toxic pathways, thus acting as a neuroprotective function in Alzheimer’s disease. Researchers in Australia have designed a novel AAV-based gene therapy approach targeting p38γ, DBA/2.p38γCA, in murine models of epilepsy in which tau is known to play a neurotoxic effect.