Mechanistically, overexpression of PTPN11 increases resistance to tyrosine kinase inhibitors (TKI) in either EGFR mutant or EGFR wild-type NSCLC cells through Erk-AKT- nuclear factor kappa B (NF-κB) and GSK3β-β-Catenin signaling pathway-mediated C-X-C motif chemokine ligand 8 (CXCL8)-chemokine receptor 1/2 (CXCR1/2) feedback loop that promotes stemness and tumorigenesis (45, 46). The gene discussed is EGFR; the disease is non-small cell lung carcinoma.