Recent technological advances in genomic analysis have revealed numerous genetic alterations involving key pathway components in receptor tyrosine kinase signaling, mTOR signaling, oxidative stress response, proliferation and cell cycle progression, which lead to oncogenic transformation in this disease.31 We primarily focus on driver gene variations (also known as oncogene addiction) in NSCLC, such as KRAS, EGFR, anaplastic lymphoma kinase (ALK), ROS1, BRAF, HER-2, MET, NTRK and RET mutations, as these can serve as therapeutic targets. The gene discussed is KRAS; the disease is non-small cell lung carcinoma.