In addition, in lung cancer, exposure to IL-1β decreases phosphatase and tensin homolog (PTEN) expression, phosphoinositide 3-kinase (PI3K)/AKT signaling activation, and the induction of epithelial–mesenchymal transition (EMT), conferring primary lung carcinoma cells with the ability to mobilize, invade, and damage distant sites, leading to angiogenesis [9,19,20]. The gene discussed is IL1B; the disease is lung carcinoma.