In our study, we found that the activation of AIM2 inflammasome in IPF PBMCs led to IL-1α, but not IL-1β, and TGF-β release in a TLR4-/caspase-1-/caspase-8-/calpain-independent manner, concomitantly to caspase-4 extracellular release. Here, IL1A is linked to idiopathic pulmonary fibrosis.