Based on the above, we suggest that AhR may induce proliferation of lung cancer cells through mechanisms involving both non-genomic activation of EGFR, and genomic activation of NF-κB and its target genes such as TMPRSS2, leading to inflammatory responses regulated by members of the IL-1 cytokine family, such as IL-1β and IL-18. This evidence concerns the gene IL1B and lung carcinoma.