In particular, receptor tyrosine kinases (RTKs) such as the epidermal growth factor receptor (EGFR) are frequently mutated or overexpressed in NSCLC, contributing to sustained proliferative signaling and therapy resistance through the activation of the RAS-RAF-MEK-ERK and PI3K-AKT-mTOR pathways [6,7,8]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.