It is tempting to speculate that these species-specific differences could be, in part, mediated by differential CARD8 inflammasome activation, which in turn influences the extent of CD4+ T cell depletion, chronic immune activation, and bystander cell immunopathology – key pathogenic events that drive the progression to AIDS in the absence of antiretroviral therapy (Kaur et al., 1998; Keele et al., 2009; Paiardini and Müller-Trutwin, 2013). This evidence concerns the gene CARD8 and AIDS.