Along the line of inflammation, because caspase-8 activated by stimulation of TLR3 or TLR4 mediates the processing of pro-IL-1β [46], it is also tempting to speculate that a TLR4/caspase-8/IL-1β pathway is activated during infection, activating caspase-3 and releasing IL-1β, which, although can produce acute inflammation, can also contribute to the non-resolution of inflammation [60]. The gene discussed is IL1B; the disease is infection.