Although cancers may have many genetic alterations, there are only a few 
mutations actually associated with essential traits of cancer cells such as cell 
proliferation or evasion from apoptosis. Because cancer cells are "addicted" to 
these "drive genes" , pharmacologic inhibition of these gene function is highly 
effective. Epidermal growth factor receptor(EGFR)-tyrosine kinase 
inhibitor(TKI)(such as gefitinib or erlotinib)treatment of lung cancer harboring 
EGFR gene mutation is one of the prototypes of such therapies. Several clinical 
trials clearly demonstrated that progression-free survival of patients treated 
with EGFR-TKI is significantly longer than that of those treated by conventional 
platinum doublet chemotherapy. EGFR-TKI therapy dramatically changed the 
paradigm of lung cancer treatment. Furthermore, in 2012, crizotinib was approved 
for lung cancer treatment with anaplastic lymphoma kinase(ALK)gene 
translocation. Targeted therapies for lung cancers "addicted" to other driver 
gene mutations including ROS1, RET or HER2 are also under development. Through 
these personalized approaches, lung cancer is changing from an acute fatal 
disease to a more chronic disease, and eventually we might be able to cure it.