Lung cancer is one of the most common malignancies, with 1.6 million new lung cancer diagnoses each year, and it is also the leading cause of death among cancer patients, with 1.4 million people dying from lung cancer each year. Treatments targeting mutations in the susceptibility gene EGFR and activation of other oncogenes have led to better outcomes for patients with more advanced NSCLC, but these therapies have not improved survival rates, and researchers continue to search for novel therapeutic approaches. Tumorigenesis is not only due to the nature of cancer cells, but also the interaction between cancer cells and the immune system plays an important role. There are many immunotherapies used clinically for cancer treatment, such as Sipuleucel-T (a vaccine that inhibits metastasis of prostate cancer cells), Ipilimumab and interleukin-2 (IL-2) (for advanced melanoma), and interleukin-2 (IL-2) (for renal cell carcinoma). However, due to the poor efficacy of treatment with BCG, interleukin-2(IL-2) and interferon, NSCLC was once considered to be an immunologically inactive tumor. However, with the successful development of a new generation of cancer vaccines and immunomodulators, immunotherapy for NSCLC has attracted renewed interest. Although the promise of vaccine therapy was seen in early studies, the results of many phase III clinical trials have been unsatisfactory. Tecemotide (START study) and belagenpumatucel-L (STOP study), conducted at local technologically advanced sites, as well as studies conducted at complementary sites, suggest no therapeutic effect. Due to genetic and epigenetic differences, the expression of cancer cell antigens differs from the expression of host cell antigens. The first step in the clearance of cancer cells by the immune system is the ability to recognize tumor cells. The T cell-mediated immune response is regulated in both directions by activating and inhibiting signals. Immune costimulatory molecules include CD28, CD137, glucocorticoid-induced tumor necrosis factor (TNF) receptor (GITR) and OX-40. Negative regulatory molecules, immune checkpoint molecules, prevent excessive activation of the immune response. Checkpoint molecules (co-suppressor molecules) include cytotoxic T lymphocyte antigen-4 (CTLA-4), programmed death 1 (PD-1), TIM3, lymphocyte activation gene 3 (LAG3) and killer cell immunoglobulin receptor (KIR). Under normal physiological conditions, these immune checkpoints protect the body from autoimmunity and inflammation. In the tumor state, these immune checkpoint proteins do not function properly, thus causing tumor tolerance and ultimately allowing tumor cells to escape from the immune system. The use of antibodies targeting these molecules for immunomodulation is increasingly being studied, and some of them have yielded promising results. Dr. Raghav Sundar from the Institute of Oncology, National University of Singapore (NUS), et al. have reviewed the modulation of the body’s immune response to tumors by costimulatory and co-suppressive molecules and recently developed therapeutic approaches, which were recently published in the journal Lung Cancer.