In addition to T790M, NSCLC patients acquire resistance to EGFR TKIs by upregulating alternative signaling mechanisms, such as PI3K/AKT/mTOR and JAK2/STAT3 pathways, epithelial–mesenchymal transition (EMT) phenotypic transformation, and several other receptor tyrosine kinases (RTKs), such as c-MET, IGF-1 receptor human epidermal HER2, and HER3 [9,12]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.