In addition, to explore the mechanism of COL8A1 upregulated IFIT1 and IFIT3-medicated EGFR activation, we overexpressed COL8A1 in lung cancer cells H1299 and H1975, and found that IFIT1, IFIT3 and pEGFR were upregulated by COL8A1 overexpression, whereas after co-transfected with COL8A1-overexpressing vectors and siIFIT1/siIFIT3, the expression of IFIT1, IFIT3 and pEGFR were suppressed, which indicated that COL8A1 promoted EGFR activation through upregulating IFIT1 and IFIT3 in lung cancer cells (Supplementary Figure 2). The gene discussed is EGFR; the disease is lung cancer.