Inflammation is a risk factor for the development of many types of neoplasia, including skin, colon, gastric, and mammary cancers, among others. Chronic pulmonary diseases, such as chronic bronchitis and asthma, predispose to lung neoplasia. We will review the mouse literature examining the role of inflammation in lung neoplasia, focusing specifically on genetic susceptibility, pharmacologic modulation of inflammatory pathways, and both transgenic and knockout mouse models used to assess pro- and anti-inflammatory pathways involved in lung neoplasia. Identification of molecular mechanisms that govern the association between inflammation and pulmonary neoplasia could provide novel preventive, diagnostic, and therapeutic strategies for a disease in which few biomarkers currently exist.