Notably, treatment of IPF PBMCs with LPS and/or LPS + ATP, well-known activators of NLRP3, led to the release of IL-1α in an NLRP3-/caspase-1/caspase-8-/TLR4- and calpain-independent manner, leading to a slight increase of caspase-4 release. The gene discussed is IL1A; the disease is idiopathic pulmonary fibrosis.