In contrast, treatment with poly(dA:dT) allowed interactions between endogenous ASC, AIM2 and caspase-1, but not Pyrin, ZBP1, caspase-8, RIPK3, RIPK1 or FADD (Fig. 4e), suggesting that infection has a distinct ability to form this AIM2 multi-protein cell death-inducing complex. This evidence concerns the gene CASP1 and infection.