EGFR and lung carcinoma: GSEA also showed that the genes enriched in the Notch, cytokine and Fc_epsilon_RI signaling pathways were abundant in the smoking group (Supplementary Fig. 4f), while the genes upregulated in non-smoking group could activate EGFR tyrosine kinase inhibitor (EGFR-TKI) resistance, ErbB (contributing to resistance to radiation and chemotherapy in cancer), PPAR, Wnt pathways and ECM-receptor interactions (a known pathway contributing to the non-smoking lung cancer) (Supplementary Fig. 4g).