Over the past few decades, advances in the understanding of NSCLC tumor biology and the identification of actionable oncogenic driver mutations have led to the development and adoption of targeted therapies for subsets of patients, such as those with aberrations in genes for the epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), B—rapidly accelerated fibrosarcoma (BRAF), ROS1 receptor tyrosine kinase and/or neurotrophic tyrosine receptor kinase (NTRK) 1/2/3 [7]. Here, EGFR is linked to neoplasm.