Next, we demonstrated a role for the pore-forming substrate of Casp1 and -11, GSDMD, since GsdmD-/- BMDMs demonstrated a partial reduction in IL-1β production following ΔpknF mutant infection after 20 hpi when compared to wild-type BMDMs (Fig 4F) but no differences were observed for cell death (Fig 4G). The gene discussed is IL1B; the disease is infection.