The crucial work performed by Heneka and coworkers demonstrated that knocking out the NLRP3 or caspase-1 genes (Nlrp3−/− or Casp-1−/−) in a mouse model of AD (APP/PS1 mice) resulted in reduced Aβ plaque deposition, decreased IL-1β levels, and ameliorated cognitive deficits compared to AD mice with intact genes. The gene discussed is CASP1; the disease is Alzheimer disease.