These results indicate that AIM2 inflammasome activation in IPF-derived PBMCs leads to IL-1α release in a caspase-1-/caspase-8- and TLR4-independent manner, implying the involvement of another mechanism(s), as observed for LPS ± ATP (Figure 2), most likely due to the non-canonical inflammasome (caspase-4 dependent). Here, AIM2 is linked to idiopathic pulmonary fibrosis.