<p>Lung cancer constitutes one of the most imperative international health crises of the twenty first century with millions of diagnosed cases and millions more of death being reported every year. Despite tobacco smoking being implicated as the leading of lung cancer incidence, a plethora of reasons including second degree smoking, pollution, exposure to carcinogens and genetic predisposition have been associated with lung cancer, particularly amongst non-smokers. Lung cancer is categorized into two key classes namely small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). Although SCLC is less prevalent than NSCLC, this malignancy is more aggressive in terms of pathogenesis. Developing effective and comprehensive therapeutic strategies is indeed the imperative need of the hour due the high mortality of the disease. Mutations in a host of genes including receptor tyrosine kinases (such as EGFR), protooncogenes (such as KRAS and ROS1), insulin receptor family (such as ALK) have been linked to lung cancer prevalence. Furthermore, cell signalling pathways (such as RAS/RAF/MEK/ERK pathway, Phosphatidylinositol 3-Kinase/AKT/PTEN pathway) and inactivation of tumour suppressor genes (such as TP53) have also been implicated in lung cancer incidence. In addition to existing treatment strategies including chemotherapy and radiation, new strategies are emerging to tackle this global menace. These include immunotherapy, vaccine development, use of nanomedicine as well as targeted gene therapy. As more novel therapeutic strategies continue to emerge, there is pressing need for a concerted global endeavour to elucidate the epigenetic and genetic mechanisms for lung cancer occurrence.</p>