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In adenocarcinoma of the lung (ADC), identification of somatic gene mutations, amplifications, or fusions of oncogenes, such as receptor tyrosine kinases, has facilitated development of targeted agents with small molecule kinase inhibitors or therapeutic monoclonal antibodies 2

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Immune checkpoint molecules like PD-1 (programmed death-1) and CTLA-4 (Cytotoxic T lymphocyte-associated antigen-4) function as negative regulators of immune activation, and when triggered by tumor or tumor-associated cells, they suppress immune responses (105, 125–128)