Eighty-five percent of patients with lung cancer present with non-small cell lung
cancer (NSCLC). Targeted therapy approaches are promising treatments for lung cancer.
However, despite the development of targeted therapies using tyrosine kinase inhibitors (TKI)
as well as monoclonal antibodies, the five-year relative survival rate for lung cancer patients
is still only 18%, and patients inevitably become resistant to therapy. Mutations in Kirsten ras
sarcoma viral homolog (KRAS) and epidermal growth factor receptor (EGFR) are the two
most common genetic events in lung adenocarcinoma; they account for 25% and 20% of
cases, respectively. Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine
kinase, and ALK rearrangements are responsible for 3–7% of NSCLC, predominantly of the
adenocarcinoma subtype, and occur in a mutually exclusive manner with KRAS and EGFR
mutations. Among drug-resistant NSCLC patients, nearly half exhibit the T790M mutation in
exon 20 of EGFR. This review focuses on some basic aspects of molecules involved in
NSCLC, the development of resistance to treatments in NSCLC, and advances in lung cancer
therapy in the past ten years. Some recent developments such as PD-1-PD-L1 checkpointbased
immunotherapy for NSCLC are also covered.