Lung cancer is a malignant tumor characterized by abnormal cell growth in the tissue lining of the lung. It is categorized into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) depending on its cell type. NSCLC accounts for approximately 80% of all lung cancers, with adenocarcinoma comprising 40% of all cases [1]. Mutator phenotype and induction of genomic instability are the key events in the early stages of cancer. The comprehensive molecular investigation of NSCLC has enabled the identification of key genes critical to the carcinogenesis process [2]. The significant genes are epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), echinoderm microtubule-associated protein-like four anaplastic lymphoma kinase (EML4-ALK), and phospholipase A2 group IIA (PLA2G2A) [3, 4]. Among these genes, 10–40% of NSCLC patients exhibit an active mutation in the EGFR gene. The EGFR family of genes belongs to the receptor tyrosine kinase family and comprises four known members: EGFR or HER1/ErbB1, HER2/ErbB2, HER3/ErbB3, and HER4/ErbB4 [4]. Among these, EGFR and HER2 are the key receptors that possess an intracellular protein kinase domain with tyrosine kinase activity, which are expressed in lung cancer. The amplification or overexpression of both genes has been associated with the clinical course of several cancers, including non-small cell lung cancer.