| Inflammation [43–49] | COX-2, NF-κB, IL-1β, IL-6, STAT3, neutrophil elastase, IL-8/neutrophil |
| MIF/macrophage | |
| Mutation and polymorphisms [48, 50–54] | Kras, p53, p16, GSTM1, CYP2A6, nAChR, HHIP, GYPA |
| Methylation [44–56] | IL-12Rβ2, Wif-1, p16, DNMT1 |
| Overexpression [55] | HER2 |
| MMPs [19, 57] | MMP-1, MMP-2, MMP-12 |
| Hypoxia/angiogenesis [44] | HIF1-α, HIF2-α, VEGF |
| Cell cycle regulator [44] | p21 |
| Adhesion molecules [44] | Galectin-3 |
| Others [58–60] | α1-ATD allele, FAM13A |
COX: cyclo-oxygenase; NF: nuclear transcription factor; IL: interleukin; STAT3: signal transducer and activator of transcription 3; MIF: macrophage migration inhibitory factor; GSTM1: glutathione S-transferase μ1; nAChR: nicotinic acetylcholine receptor; HHIP: Hedgehog-interacting protein; GYPA: glycophorin A; IL-12R: interleukin-12 receptor; Wif-1: WNT inhibitory factor 1; DNMT1: DNA methyltransferase 1; HER2: human EGFR-related 2; MMP: matrix metalloproteinase; HIF: hypoxia inducible factor; VEGF: vascular endothelial growth factor; α1-ATD: α1-antitrypsin deficiency; FAM13A: family with sequence similarity 13 member A.