Moreover, the brains of FTD‐tau patients showed elevated expression levels of p75NTR and proNGF, while knockdown of p75NTR in P301L tau transgenic mice attenuated the proNGF‐induced tau hyperphosphorylation via activation of the Akt/GSK‐3β pathway (Shen et al. 2018; Mañucat‐Tan et al. 2019). The gene discussed is MAPT; the disease is frontotemporal dementia.