Because EGFR-TKI-resistant lung cancer cell lines (HCC827 GR, H1993 ER, and H292 ER) acquired resistance via stepwise exposure to EGFR-TKIs over a long-term period [21, 27] and exhibited downregulated signaling activity of EGFR (Figure 1(d)), compensatory activation of mitochondrial OXPHOS in the resistant NSCLC cell lines appears reasonable. This evidence concerns the gene EGFR and lung carcinoma.