As an example, work in wtEGFR-expressing cancer cells highly resistant to EGFR-TKIs (Hela-R30 and OSCC 686LN), in which autophagy is not robustly activated, showed that rapamycin, an mTOR inhibitor, both restored autophagy in these cells and augmented the cytotoxic effect of EGFR-TKIs [143]. This evidence concerns the gene EGFR and cancer.