Resistance to anti-EGFR TKI monotherapy has been linked to c-MET overexpression, while c-MET TKI monotherapy triggers upregulation and phosphorylation of EGFR, suggesting compensatory receptor tyrosine kinase (RTK) signaling in TNBC and NSCLC [11, 12]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.