Genetic or pharmacological inhibition of NLRP3 has recently been shown to rescue cognitive impairment in mouse models of FTD-tau, supporting the possibility of NLRP3 inhibition as a useful therapeutic strategy.60,61 NLRP3 is also linked to tau seeding and aggregation, with NLRP3 inhibition reducing pathological burden in tau transgenic mice.59,60 Further work is required to determine the contribution of GR-induced NLRP3 activation to disease pathogenesis in C9FTD/ALS. The gene discussed is MAPT; the disease is frontotemporal dementia.