We have recently shown that β-arrestin2 is also increased in frontotemporal lobar degeneration (FTLD-tau) patients (Woo et al, 2020), and genetic reduction in β-arrestin2 or expression of dominant-negative mutants that decreases β-arrestin2 oligomer formation, significantly mitigates tauopathy in vivo (Woo et al, 2020). The gene discussed is MAPT; the disease is frontotemporal dementia.