Taken together, these data suggest that IPF-derived PBMCs are able to release IL-1α after LPS and/or LPS + ATP stimulation in an NLRP3-/caspase-1-/caspase-8-, TLR4-, and calpain-independent manner, but most likely via the involvement of caspase-4. Here, IL1A is linked to idiopathic pulmonary fibrosis.