In addition, the EGFR-TKI resistance mechanisms of multiple cancers, including breast cancer, may be due to compensatory activation of other receptor tyrosine kinases, such as MET, AXL or IGF1R, which are overexpressed and activate downstream survival pathways (such as AKT, NF-κB and ERK) to help cancer cells escape from cell death following erlotinib or gefitinib treatment, as observed in lung cancer cells [10, 32, 41–43]. This evidence concerns the gene AKT1 and breast carcinoma.