Notably, unlike other live-pathogen infections [9, 12–14, 24–26], while these secondary cell death pathways are AIM2 dependent, they are not mediated through direct interactions with apoptosis- and necroptosis-related molecules, such as CASP8 or RIPK3, suggesting a broader network of signaling interactions downstream of AIM2 activation. The gene discussed is AIM2; the disease is infection.