Notably, pharmacological blockade or genetic deletion of NLRP3, caspase-1, IL-1β, or C-C motif chemokine ligand 2 (CCL2), which contribute to the recruitment of circulating bone marrow-derived monocytes and to the replenishment and pro-inflammatory phenotype of lung macrophages, almost completely abrogated the lung cancer-promoting effect of HDM in our models. The gene discussed is CCL2; the disease is lung cancer.