Relevant to lung cancer, our previous studies have shown that exposure to cigarette smoke generates PAF agonists in a PAFR-dependent manner that induce systemic immunosuppression in a process blocked by antioxidants, cyclooxygenase types 2 (COX-2) inhibitors, and PAF-metabolizing enzyme PAF-acetyl hydrolase (PAF-AH), as well as depleting antibodies against immunosuppressive regulatory T cells (Tregs) [32]. This evidence concerns the gene PTAFR and lung carcinoma.