In addition, Zheng et al. (2021) found that overexpression of USP25 leads to microglia activation and inflammation, further induces synaptic and cognitive deficits, and silencing of the USP25 gene attenuates the neuroinflammatory response induced by microglia activation, restores microglia homeostasis, and improves synaptic elimination, which then restores cognitive function in AD model animals. The gene discussed is USP25; the disease is Alzheimer disease.