Although the CASP8/RIPK3 axis drives various inflammatory PCDs during live-pathogen infections, such as HSV1 [9], Francisella novicida [9], influenza A virus [12, 13], murine hepatitis virus [14, 24], and PAMPs/DAMPs [25, 26], there was no significant discrepancy in cell death, IL-1β, or IL-18 release among WT, Ripk3–/–, and Ripk3–/–Casp8–/– iBMDMs upon MPXV infection (Fig. 4A–D). Here, IL18 is linked to infection.