EGFR-mutant NSCLC cells with increased EGFR tyrosine kinase activity excessively activate multiple EGFR-mediated downstream signaling pathways, such as MAPK, PI3K/AKT, and STAT3 pathways, consequently promoting the overexpression of CSC biomarkers and enhancing the stem-like properties of the cells [32,33,34,52]. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.